Electroacupuncture Improves Neuronal Damage and Mitochondrial Dysfunction Through the TRPC1 and SIRT1/AMPK Signaling Pathways to Alleviate Parkinson’s Disease in Mice

Parkinson’s disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body’s own immunity and disease resista...

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Published inJournal of molecular neuroscience Vol. 74; no. 1; p. 5
Main Authors Geng, Xin, Zou, Yanghong, Huang, Tao, Li, Shipeng, Pang, Ailan, Yu, Hualin
Format Journal Article
LanguageEnglish
Published New York Springer US 08.01.2024
Springer Nature B.V
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Abstract Parkinson’s disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body’s own immunity and disease resistance. This study mainly discusses the specific mechanism underlying electroacupuncture intervention in improving PD. Male C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a mouse PD model, and the chorea trembling control area of the head of PD mice was treated by electroacupuncture. Western blotting was used to detect the expression of related proteins in mouse pathological samples; TUNEL measured neuronal apoptosis levels; Nissl staining observed neuronal damage; immunofluorescence and immunohistochemistry were used to detect the expression of Iba-1, TH, and α-syn in substantia nigra denser (SN). The expression levels of oxidative stress factors and inflammatory factors were measured by kits. Flow cytometry measured mitochondrial membrane potential and Ca 2+ levels. MPTP intraperitoneal injection induced an increase in inflammatory factors in PD mice and promoted the oxidative stress response, and the inflammatory response was alleviated after electroacupuncture treatment. Electroacupuncture intervention effectively alters the decrease in oxidative stress levels and alleviates neuronal damage in PD mice. Electroacupuncture improves mitochondrial dysfunction induced by MPTP in PD mice by activating the SIRT1/AMPK signaling pathway. We also confirmed that knocking down TRPC1 can inhibit the SIRT1/AMPK signaling pathway, weaken the Ca 2+ content in mouse neuronal tissue, and promote cell apoptosis. Electroacupuncture improves neuronal damage and alleviates PD in mice through the TRPC1 and SIRT1/AMPK signaling pathways. In addition, electroacupuncture therapy can improve MPTP-induced mitochondrial dysfunction in PD mice and alleviate the PD process.
AbstractList Parkinson’s disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body’s own immunity and disease resistance. This study mainly discusses the specific mechanism underlying electroacupuncture intervention in improving PD. Male C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a mouse PD model, and the chorea trembling control area of the head of PD mice was treated by electroacupuncture. Western blotting was used to detect the expression of related proteins in mouse pathological samples; TUNEL measured neuronal apoptosis levels; Nissl staining observed neuronal damage; immunofluorescence and immunohistochemistry were used to detect the expression of Iba-1, TH, and α-syn in substantia nigra denser (SN). The expression levels of oxidative stress factors and inflammatory factors were measured by kits. Flow cytometry measured mitochondrial membrane potential and Ca 2+ levels. MPTP intraperitoneal injection induced an increase in inflammatory factors in PD mice and promoted the oxidative stress response, and the inflammatory response was alleviated after electroacupuncture treatment. Electroacupuncture intervention effectively alters the decrease in oxidative stress levels and alleviates neuronal damage in PD mice. Electroacupuncture improves mitochondrial dysfunction induced by MPTP in PD mice by activating the SIRT1/AMPK signaling pathway. We also confirmed that knocking down TRPC1 can inhibit the SIRT1/AMPK signaling pathway, weaken the Ca 2+ content in mouse neuronal tissue, and promote cell apoptosis. Electroacupuncture improves neuronal damage and alleviates PD in mice through the TRPC1 and SIRT1/AMPK signaling pathways. In addition, electroacupuncture therapy can improve MPTP-induced mitochondrial dysfunction in PD mice and alleviate the PD process.
Parkinson's disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body's own immunity and disease resistance. This study mainly discusses the specific mechanism underlying electroacupuncture intervention in improving PD. Male C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a mouse PD model, and the chorea trembling control area of the head of PD mice was treated by electroacupuncture. Western blotting was used to detect the expression of related proteins in mouse pathological samples; TUNEL measured neuronal apoptosis levels; Nissl staining observed neuronal damage; immunofluorescence and immunohistochemistry were used to detect the expression of Iba-1, TH, and α-syn in substantia nigra denser (SN). The expression levels of oxidative stress factors and inflammatory factors were measured by kits. Flow cytometry measured mitochondrial membrane potential and Ca2+ levels. MPTP intraperitoneal injection induced an increase in inflammatory factors in PD mice and promoted the oxidative stress response, and the inflammatory response was alleviated after electroacupuncture treatment. Electroacupuncture intervention effectively alters the decrease in oxidative stress levels and alleviates neuronal damage in PD mice. Electroacupuncture improves mitochondrial dysfunction induced by MPTP in PD mice by activating the SIRT1/AMPK signaling pathway. We also confirmed that knocking down TRPC1 can inhibit the SIRT1/AMPK signaling pathway, weaken the Ca2+ content in mouse neuronal tissue, and promote cell apoptosis. Electroacupuncture improves neuronal damage and alleviates PD in mice through the TRPC1 and SIRT1/AMPK signaling pathways. In addition, electroacupuncture therapy can improve MPTP-induced mitochondrial dysfunction in PD mice and alleviate the PD process.Parkinson's disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body's own immunity and disease resistance. This study mainly discusses the specific mechanism underlying electroacupuncture intervention in improving PD. Male C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a mouse PD model, and the chorea trembling control area of the head of PD mice was treated by electroacupuncture. Western blotting was used to detect the expression of related proteins in mouse pathological samples; TUNEL measured neuronal apoptosis levels; Nissl staining observed neuronal damage; immunofluorescence and immunohistochemistry were used to detect the expression of Iba-1, TH, and α-syn in substantia nigra denser (SN). The expression levels of oxidative stress factors and inflammatory factors were measured by kits. Flow cytometry measured mitochondrial membrane potential and Ca2+ levels. MPTP intraperitoneal injection induced an increase in inflammatory factors in PD mice and promoted the oxidative stress response, and the inflammatory response was alleviated after electroacupuncture treatment. Electroacupuncture intervention effectively alters the decrease in oxidative stress levels and alleviates neuronal damage in PD mice. Electroacupuncture improves mitochondrial dysfunction induced by MPTP in PD mice by activating the SIRT1/AMPK signaling pathway. We also confirmed that knocking down TRPC1 can inhibit the SIRT1/AMPK signaling pathway, weaken the Ca2+ content in mouse neuronal tissue, and promote cell apoptosis. Electroacupuncture improves neuronal damage and alleviates PD in mice through the TRPC1 and SIRT1/AMPK signaling pathways. In addition, electroacupuncture therapy can improve MPTP-induced mitochondrial dysfunction in PD mice and alleviate the PD process.
Parkinson’s disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body’s own immunity and disease resistance. This study mainly discusses the specific mechanism underlying electroacupuncture intervention in improving PD. Male C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a mouse PD model, and the chorea trembling control area of the head of PD mice was treated by electroacupuncture. Western blotting was used to detect the expression of related proteins in mouse pathological samples; TUNEL measured neuronal apoptosis levels; Nissl staining observed neuronal damage; immunofluorescence and immunohistochemistry were used to detect the expression of Iba-1, TH, and α-syn in substantia nigra denser (SN). The expression levels of oxidative stress factors and inflammatory factors were measured by kits. Flow cytometry measured mitochondrial membrane potential and Ca2+ levels. MPTP intraperitoneal injection induced an increase in inflammatory factors in PD mice and promoted the oxidative stress response, and the inflammatory response was alleviated after electroacupuncture treatment. Electroacupuncture intervention effectively alters the decrease in oxidative stress levels and alleviates neuronal damage in PD mice. Electroacupuncture improves mitochondrial dysfunction induced by MPTP in PD mice by activating the SIRT1/AMPK signaling pathway. We also confirmed that knocking down TRPC1 can inhibit the SIRT1/AMPK signaling pathway, weaken the Ca2+ content in mouse neuronal tissue, and promote cell apoptosis. Electroacupuncture improves neuronal damage and alleviates PD in mice through the TRPC1 and SIRT1/AMPK signaling pathways. In addition, electroacupuncture therapy can improve MPTP-induced mitochondrial dysfunction in PD mice and alleviate the PD process.
Parkinson's disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a major challenge in the clinical field. Acupuncture therapy has been shown in many studies to enhance the body's own immunity and disease resistance. This study mainly discusses the specific mechanism underlying electroacupuncture intervention in improving PD. Male C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a mouse PD model, and the chorea trembling control area of the head of PD mice was treated by electroacupuncture. Western blotting was used to detect the expression of related proteins in mouse pathological samples; TUNEL measured neuronal apoptosis levels; Nissl staining observed neuronal damage; immunofluorescence and immunohistochemistry were used to detect the expression of Iba-1, TH, and α-syn in substantia nigra denser (SN). The expression levels of oxidative stress factors and inflammatory factors were measured by kits. Flow cytometry measured mitochondrial membrane potential and Ca levels. MPTP intraperitoneal injection induced an increase in inflammatory factors in PD mice and promoted the oxidative stress response, and the inflammatory response was alleviated after electroacupuncture treatment. Electroacupuncture intervention effectively alters the decrease in oxidative stress levels and alleviates neuronal damage in PD mice. Electroacupuncture improves mitochondrial dysfunction induced by MPTP in PD mice by activating the SIRT1/AMPK signaling pathway. We also confirmed that knocking down TRPC1 can inhibit the SIRT1/AMPK signaling pathway, weaken the Ca content in mouse neuronal tissue, and promote cell apoptosis. Electroacupuncture improves neuronal damage and alleviates PD in mice through the TRPC1 and SIRT1/AMPK signaling pathways. In addition, electroacupuncture therapy can improve MPTP-induced mitochondrial dysfunction in PD mice and alleviate the PD process.
ArticleNumber 5
Author Yu, Hualin
Geng, Xin
Huang, Tao
Pang, Ailan
Zou, Yanghong
Li, Shipeng
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CitedBy_id crossref_primary_10_1016_j_ctim_2024_103045
crossref_primary_10_1152_jn_00497_2024
crossref_primary_10_1016_j_jtcme_2024_09_002
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Keywords Mitochondrial dysfunction
Electroacupuncture
SIRT1/AMPK
TRPC1
Parkinson’s disease
Language English
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crossref_citationtrail_10_1007_s12031_023_02186_z
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PublicationDate 2024-01-08
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  year: 2024
  text: 2024-01-08
  day: 08
PublicationDecade 2020
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PublicationTitle Journal of molecular neuroscience
PublicationTitleAbbrev J Mol Neurosci
PublicationTitleAlternate J Mol Neurosci
PublicationYear 2024
Publisher Springer US
Springer Nature B.V
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JinMMatsumotoSAyakiTDOPAnization of tyrosine in α-synuclein by tyrosine hydroxylase leads to the formation of oligomers [J]Nat Commun202213168801:CAS:528:DC%2BB38XivFSisr7I10.1038/s41467-022-34555-4363714009653393
XuNMengHLiuTTRPC1 deficiency exacerbates cerebral ischemia/reperfusion-induced neurological injury by potentiating Nox4-derived reactive oxygen species generation [J]Cell Physiol Biochem2018514172317381:CAS:528:DC%2BC1cXisFWrtLzO10.1159/00049567630504729
He XL, Li XZ, Xu DW et al (2023) Electroacupuncture intervention improves lipid metabolism and promotes browning of white adipose tissue by activating AMPK/Sirt1 pathway and up-regulating Nrg4 content in middle-aged and aged obese rats [J]. Zhen ci yan jiu = Acupunct Res 48(8):764–72
NguyenMWongYCYsselsteinDSynaptic, mitochondrial, and lysosomal dysfunction in Parkinson’s disease [J]Trends Neurosci20194221401491:CAS:528:DC%2BC1cXit1CrtrbF10.1016/j.tins.2018.11.00130509690
LeeYLeeHBaeCHElectroacupuncture at GB34 modulates neurogenesis and BDNF-ERK signaling in a mouse model of Parkinson’s disease [J]J Tradit Complement Med20231332632691:CAS:528:DC%2BB3sXos1Ght7w%3D10.1016/j.jtcme.2023.01.0053712819110148113
Huang K, Bao CL, Chen WW et al (2021) Effect of electroacupuncture on mitochondrial function in mice with Parkinson’s disease [J]. Zhen ci yan jiu = Acupunct Res 46(1):21–6
Yu Y, Zhan X, Cong Y et al (2016) The role of TRP and trkA signal transduction pathways in the neuroprotective mechanism of electroacupuncture in Parkinson’s disease [M]. Weihai Wendeng Central Hospital
ZhangCZhaoMWangBThe Nrf2-NLRP3-caspase-1 axis mediates the neuroprotective effects of celastrol in Parkinson’s disease [J]Redox Biol2021471:CAS:528:DC%2BB3MXitFCrsLvP10.1016/j.redox.2021.102134346003348487081
Amores-Bonet L, Kleener R, Theis T et al (2022) Interactions between the polysialylated neural cell adhesion molecule and the transient receptor potential canonical channels 1, 4, and 5 induce entry of Ca(2+) into neurons [J]. Int J Mol Sci 23(17):10027
WangHChengXTianJTRPC channels: Structure, function, regulation and recent advances in small molecular probes [J]Pharmacol Ther20202091:CAS:528:DC%2BB3cXjs1Krsrw%3D10.1016/j.pharmthera.2020.107497320045137183440
ArshadAChenXCongZTRPC1 protects dopaminergic SH-SY5Y cells from MPP+, salsolinol, and N-methyl-(R)-salsolinol-induced cytotoxicity [J]Acta Biochim Biophys Sin (shanghai)201446122301:CAS:528:DC%2BC2cXhs1Gluw%3D%3D10.1093/abbs/gmt12724252728
Wu S, Zou MH (2020) AMPK, mitochondrial function, and cardiovascular disease [J]. Int J Mol Sci 21(14):4987
Olsen AL, Clemens SG, Feany MB (2022) Nicotine-mediated rescue of α-synuclein toxicity requires synaptic vesicle glycoprotein 2 in drosophila [J]. Mov Disord 38(2):244–255
Zhang N, Yu X, Song L et al (2022) Ferritin confers protection against iron-mediated neurotoxicity and ferroptosis through iron chelating mechanisms in MPP(+)-induced MES23.5 dopaminergic cells [J]. Free Radic Biol Med 193(Pt 2):751–763
Lam CH, Cheung JK, Tse DY et al (2022) Proteomic profiling revealed mitochondrial dysfunction in photoreceptor cells under hyperglycemia [J]. Int J Mol Sci 23(21):13366
Zou Y, Chen Z, Sun C et al (2021) Exercise intervention mitigates pathological liver changes in NAFLD zebrafish by activating SIRT1/AMPK/NRF2 Signaling [J]. Int J Mol Sci 22(20):10940
HuangYLiuZLiNParkinson’s disease derived exosomes aggravate neuropathology in SNCA*A53T Mice [J]Ann Neurol20229222302451:CAS:528:DC%2BB38XitFCjsb%2FL10.1002/ana.2642135596947
SongLZLiYQianXParkinson’s disease constipation effect of electroacupuncture at ST25 through colonic motility and enteric neuropathology [J]Front Neurol202213109212710.3389/fneur.2022.109212736733445
GaiCQiangTZhangYElectroacupuncture in treatment of Parkinson disease: a protocol for meta-analysis and systematic review [J]Medicine2021100310.1097/MD.0000000000023010335459237837981
LizamaBNChuCTNeuronal autophagy and mitophagy in Parkinson’s disease [J]Mol Aspects Med2021821:CAS:528:DC%2BB3MXitVOls7vF10.1016/j.mam.2021.100972341308678665948
MaherPvan LeyenKDeyPNThe role of Ca(2+) in cell death caused by oxidative glutamate toxicity and ferroptosis [J]Cell Calcium20187047551:CAS:528:DC%2BC2sXot1ehtrc%3D10.1016/j.ceca.2017.05.00728545724
SunYZhangHSelvarajSInhibition of L-type Ca(2+) channels by TRPC1-STIM1 complex is essential for the protection of dopaminergic neurons [J]J Neurosci20173712336433771:CAS:528:DC%2BC2sXhtVymtL%2FE10.1523/JNEUROSCI.3010-16.2017282581685373123
ChenMPengLGongPBaicalein induces mitochondrial autophagy to prevent Parkinson’s disease in rats via miR-30b and the SIRT1/AMPK/mTOR pathway [J]Front Neurol20211210.3389/fneur.2021.64681735237220
LuZSunGFPanXABCATc inhibitor 2 ameliorated mitochondrial dysfunction and apoptosis in oleic acid-induced non-alcoholic fatty liver disease model [J]Front Pharmacol20221310255511:CAS:528:DC%2BB38XjtVSks73P10.3389/fphar.2022.1025551363862349650408
Paul S, Fatihi S, Sharma S et al (2022) Cyclin-dependent kinase 5 regulates cPLA2 activity and neuroinflammation in Parkinson’s disease [J]. eNeuro 9(6):ENEURO.0180–22.2022
HoffmannRFJonkerMRBrandenburgSMMitochondrial dysfunction increases pro-inflammatory cytokine production and impairs repair and corticosteroid responsiveness in lung epithelium [J]Sci Rep201991150471:STN:280:DC%2BB3Mjgt1Cjug%3D%3D10.1038/s41598-019-51517-x316363296803636
LeeEJChoiYLeeHJHuman neural stem cell-derived extracellular vesicles protect against Parkinson’s disease pathologies [J]J Nanobiotechnology20222011981:CAS:528:DC%2BB38Xhs1KntrrE10.1186/s12951-022-01356-2354688559040239
BairAMThippegowdaPBFreichelMCa2+ entry via TRPC channels is necessary for thrombin-induced NF-kappaB activation in endothelial cells through AMP-activated protein kinase and protein kinase Cdelta [J]J Biol Chem200928415635741:CAS:528:DC%2BD1cXhsFCjtLvF10.1074/jbc.M803984200189907072610508
EstevesMAbreuRFernandesHMicroRNA-124-3p-enriched small extracellular vesicles as a therapeutic approach for Parkinson’s disease [J]Mol Ther20223010317631921:CAS:528:DC%2BB38XhsFKjtrjE10.1016/j.ymthe.2022.06.003356893819552816
SelvarajSSunYWattJANeurotoxin-induced ER stress in mouse dopaminergic neurons involves downregulation of TRPC1 and inhibition of AKT/mTOR signaling [J]J Clin Invest20121224135413671:CAS:528:DC%2BC38Xlt1egur4%3D10.1172/JCI61332224461863314472
ZhaoYLuoDNingZElectro-acupuncture ameliorated MPTP-induced parkinsonism in mice via TrkB neurotrophic signaling [J]Front Neurosci20191349610.3389/fnins.2019.00496311563766528026
Cantó C, Gerhart-Hines Z, Feige JN et al (2009) AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity [J]. Nature 458(7241):1056–60
MohamadKAEl-NagaRNWahdanSANeuroprotective effects of indole-3-carbinol on the rotenone rat model of Parkinson’s disease: impact of the SIRT1-AMPK signaling pathway [J]Toxicol Appl Pharmacol20224351:CAS:528:DC%2BB38XjsVemug%3D%3D10.1016/j.taap.2021.11585334973289
StephensonJNutmaEvan der ValkPInflammation in CNS neurodegenerative diseases [J]Immunology201815422042191:CAS:528:DC%2BC1cXns1Wnsrc%3D10.1111/imm.12922295134025980185
WuJLuADZhangLPStudy of clinical outcome and prognosis in pediatric core binding factor-acute myeloid leukemia] [JZhonghua Xue Ye Xue Za Zhi201940152571:CAS:528:DC%2BB3cXlslOhtbY%3D30704229
EldeebMAThomasRARaghebMAMitochondrial quality control in health and in Parkinson’s disease [J]Physiol Rev20221024172117551:CAS:528:DC%2BB38XjtFCgsrzM10.1152/physrev.00041.202135466694
VaidyaBSharmaSSTransient receptor potential channels as an emerging target for the treatment of Parkinson’s disease: an insight into role of pharmacological interventions [J]Front Cell Dev Biol2020810.3389/fcell.2020.584513333304617714790
HeckmanCAAdemuyiwaOMCayerMLHow filopodia respond to calcium in the absence of a calcium-binding structural protein: non-channel functions of TRP [J]Cell Commun Signal20222011301:CAS:528:DC%2BB38Xit12js7jP10.1186/s12964-022-00927-y360288989414478
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Y Sun (2186_CR30) 2017; 37
M Jin (2186_CR15) 2022; 13
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S Selvaraj (2186_CR27) 2012; 122
M Esteves (2186_CR8) 2022; 30
P Maher (2186_CR22) 2018; 70
BN Lizama (2186_CR20) 2021; 82
RF Hoffmann (2186_CR12) 2019; 9
2186_CR41
C Gai (2186_CR9) 2021; 100
References_xml – reference: Huang K, Bao CL, Chen WW et al (2021) Effect of electroacupuncture on mitochondrial function in mice with Parkinson’s disease [J]. Zhen ci yan jiu = Acupunct Res 46(1):21–6
– reference: LeeEJChoiYLeeHJHuman neural stem cell-derived extracellular vesicles protect against Parkinson’s disease pathologies [J]J Nanobiotechnology20222011981:CAS:528:DC%2BB38Xhs1KntrrE10.1186/s12951-022-01356-2354688559040239
– reference: EstevesMAbreuRFernandesHMicroRNA-124-3p-enriched small extracellular vesicles as a therapeutic approach for Parkinson’s disease [J]Mol Ther20223010317631921:CAS:528:DC%2BB38XhsFKjtrjE10.1016/j.ymthe.2022.06.003356893819552816
– reference: Olsen AL, Clemens SG, Feany MB (2022) Nicotine-mediated rescue of α-synuclein toxicity requires synaptic vesicle glycoprotein 2 in drosophila [J]. Mov Disord 38(2):244–255
– reference: Zhang N, Yu X, Song L et al (2022) Ferritin confers protection against iron-mediated neurotoxicity and ferroptosis through iron chelating mechanisms in MPP(+)-induced MES23.5 dopaminergic cells [J]. Free Radic Biol Med 193(Pt 2):751–763
– reference: ZhaoYLuoDNingZElectro-acupuncture ameliorated MPTP-induced parkinsonism in mice via TrkB neurotrophic signaling [J]Front Neurosci20191349610.3389/fnins.2019.00496311563766528026
– reference: HuangYLiuZLiNParkinson’s disease derived exosomes aggravate neuropathology in SNCA*A53T Mice [J]Ann Neurol20229222302451:CAS:528:DC%2BB38XitFCjsb%2FL10.1002/ana.2642135596947
– reference: WangHChengXTianJTRPC channels: Structure, function, regulation and recent advances in small molecular probes [J]Pharmacol Ther20202091:CAS:528:DC%2BB3cXjs1Krsrw%3D10.1016/j.pharmthera.2020.107497320045137183440
– reference: Amores-Bonet L, Kleener R, Theis T et al (2022) Interactions between the polysialylated neural cell adhesion molecule and the transient receptor potential canonical channels 1, 4, and 5 induce entry of Ca(2+) into neurons [J]. Int J Mol Sci 23(17):10027
– reference: VaidyaBSharmaSSTransient receptor potential channels as an emerging target for the treatment of Parkinson’s disease: an insight into role of pharmacological interventions [J]Front Cell Dev Biol2020810.3389/fcell.2020.584513333304617714790
– reference: ArshadAChenXCongZTRPC1 protects dopaminergic SH-SY5Y cells from MPP+, salsolinol, and N-methyl-(R)-salsolinol-induced cytotoxicity [J]Acta Biochim Biophys Sin (shanghai)201446122301:CAS:528:DC%2BC2cXhs1Gluw%3D%3D10.1093/abbs/gmt12724252728
– reference: LuZSunGFPanXABCATc inhibitor 2 ameliorated mitochondrial dysfunction and apoptosis in oleic acid-induced non-alcoholic fatty liver disease model [J]Front Pharmacol20221310255511:CAS:528:DC%2BB38XjtVSks73P10.3389/fphar.2022.1025551363862349650408
– reference: YangSWuGLLiNA mitochondria-targeted molecular phototheranostic platform for NIR-II imaging-guided synergistic photothermal/photodynamic/immune therapy [J]J Nanobiotechnology20222014751:CAS:528:DC%2BB38XivVyqurnK10.1186/s12951-022-01679-0363690399652787
– reference: WuJLuADZhangLPStudy of clinical outcome and prognosis in pediatric core binding factor-acute myeloid leukemia] [JZhonghua Xue Ye Xue Za Zhi201940152571:CAS:528:DC%2BB3cXlslOhtbY%3D30704229
– reference: HoffmannRFJonkerMRBrandenburgSMMitochondrial dysfunction increases pro-inflammatory cytokine production and impairs repair and corticosteroid responsiveness in lung epithelium [J]Sci Rep201991150471:STN:280:DC%2BB3Mjgt1Cjug%3D%3D10.1038/s41598-019-51517-x316363296803636
– reference: LizamaBNChuCTNeuronal autophagy and mitophagy in Parkinson’s disease [J]Mol Aspects Med2021821:CAS:528:DC%2BB3MXitVOls7vF10.1016/j.mam.2021.100972341308678665948
– reference: EldeebMAThomasRARaghebMAMitochondrial quality control in health and in Parkinson’s disease [J]Physiol Rev20221024172117551:CAS:528:DC%2BB38XjtFCgsrzM10.1152/physrev.00041.202135466694
– reference: GaiCQiangTZhangYElectroacupuncture in treatment of Parkinson disease: a protocol for meta-analysis and systematic review [J]Medicine2021100310.1097/MD.0000000000023010335459237837981
– reference: LeeYLeeHBaeCHElectroacupuncture at GB34 modulates neurogenesis and BDNF-ERK signaling in a mouse model of Parkinson’s disease [J]J Tradit Complement Med20231332632691:CAS:528:DC%2BB3sXos1Ght7w%3D10.1016/j.jtcme.2023.01.0053712819110148113
– reference: ChaoCCHuangCLChengJJSRT1720 as an SIRT1 activator for alleviating paraquat-induced models of Parkinson’s disease [J]Redox Biol2022581:CAS:528:DC%2BB38XivVOnsbvF10.1016/j.redox.2022.102534363791809663539
– reference: HeckmanCAAdemuyiwaOMCayerMLHow filopodia respond to calcium in the absence of a calcium-binding structural protein: non-channel functions of TRP [J]Cell Commun Signal20222011301:CAS:528:DC%2BB38Xit12js7jP10.1186/s12964-022-00927-y360288989414478
– reference: SunYZhangHSelvarajSInhibition of L-type Ca(2+) channels by TRPC1-STIM1 complex is essential for the protection of dopaminergic neurons [J]J Neurosci20173712336433771:CAS:528:DC%2BC2sXhtVymtL%2FE10.1523/JNEUROSCI.3010-16.2017282581685373123
– reference: Cantó C, Gerhart-Hines Z, Feige JN et al (2009) AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity [J]. Nature 458(7241):1056–60
– reference: MohamadKAEl-NagaRNWahdanSANeuroprotective effects of indole-3-carbinol on the rotenone rat model of Parkinson’s disease: impact of the SIRT1-AMPK signaling pathway [J]Toxicol Appl Pharmacol20224351:CAS:528:DC%2BB38XjsVemug%3D%3D10.1016/j.taap.2021.11585334973289
– reference: MaherPvan LeyenKDeyPNThe role of Ca(2+) in cell death caused by oxidative glutamate toxicity and ferroptosis [J]Cell Calcium20187047551:CAS:528:DC%2BC2sXot1ehtrc%3D10.1016/j.ceca.2017.05.00728545724
– reference: BairAMThippegowdaPBFreichelMCa2+ entry via TRPC channels is necessary for thrombin-induced NF-kappaB activation in endothelial cells through AMP-activated protein kinase and protein kinase Cdelta [J]J Biol Chem200928415635741:CAS:528:DC%2BD1cXhsFCjtLvF10.1074/jbc.M803984200189907072610508
– reference: Lin JG, Chen CJ, Yang HB et al (2017) Electroacupuncture Promotes recovery of motor function and reduces dopaminergic neuron degeneration in rodent models of Parkinson’s disease [J]. Int J Mol Sci 18(9):1846
– reference: He XL, Li XZ, Xu DW et al (2023) Electroacupuncture intervention improves lipid metabolism and promotes browning of white adipose tissue by activating AMPK/Sirt1 pathway and up-regulating Nrg4 content in middle-aged and aged obese rats [J]. Zhen ci yan jiu = Acupunct Res 48(8):764–72
– reference: XuNMengHLiuTTRPC1 deficiency exacerbates cerebral ischemia/reperfusion-induced neurological injury by potentiating Nox4-derived reactive oxygen species generation [J]Cell Physiol Biochem2018514172317381:CAS:528:DC%2BC1cXisFWrtLzO10.1159/00049567630504729
– reference: ChenMPengLGongPBaicalein induces mitochondrial autophagy to prevent Parkinson’s disease in rats via miR-30b and the SIRT1/AMPK/mTOR pathway [J]Front Neurol20211210.3389/fneur.2021.64681735237220
– reference: SelvarajSSunYWattJANeurotoxin-induced ER stress in mouse dopaminergic neurons involves downregulation of TRPC1 and inhibition of AKT/mTOR signaling [J]J Clin Invest20121224135413671:CAS:528:DC%2BC38Xlt1egur4%3D10.1172/JCI61332224461863314472
– reference: Lam CH, Cheung JK, Tse DY et al (2022) Proteomic profiling revealed mitochondrial dysfunction in photoreceptor cells under hyperglycemia [J]. Int J Mol Sci 23(21):13366
– reference: Yu Y, Zhan X, Cong Y et al (2016) The role of TRP and trkA signal transduction pathways in the neuroprotective mechanism of electroacupuncture in Parkinson’s disease [M]. Weihai Wendeng Central Hospital
– reference: Zou Y, Chen Z, Sun C et al (2021) Exercise intervention mitigates pathological liver changes in NAFLD zebrafish by activating SIRT1/AMPK/NRF2 Signaling [J]. Int J Mol Sci 22(20):10940
– reference: SongLZLiYQianXParkinson’s disease constipation effect of electroacupuncture at ST25 through colonic motility and enteric neuropathology [J]Front Neurol202213109212710.3389/fneur.2022.109212736733445
– reference: ZhangCZhaoMWangBThe Nrf2-NLRP3-caspase-1 axis mediates the neuroprotective effects of celastrol in Parkinson’s disease [J]Redox Biol2021471:CAS:528:DC%2BB3MXitFCrsLvP10.1016/j.redox.2021.102134346003348487081
– reference: JinMMatsumotoSAyakiTDOPAnization of tyrosine in α-synuclein by tyrosine hydroxylase leads to the formation of oligomers [J]Nat Commun202213168801:CAS:528:DC%2BB38XivFSisr7I10.1038/s41467-022-34555-4363714009653393
– reference: NguyenMWongYCYsselsteinDSynaptic, mitochondrial, and lysosomal dysfunction in Parkinson’s disease [J]Trends Neurosci20194221401491:CAS:528:DC%2BC1cXit1CrtrbF10.1016/j.tins.2018.11.00130509690
– reference: Paul S, Fatihi S, Sharma S et al (2022) Cyclin-dependent kinase 5 regulates cPLA2 activity and neuroinflammation in Parkinson’s disease [J]. eNeuro 9(6):ENEURO.0180–22.2022
– reference: StephensonJNutmaEvan der ValkPInflammation in CNS neurodegenerative diseases [J]Immunology201815422042191:CAS:528:DC%2BC1cXns1Wnsrc%3D10.1111/imm.12922295134025980185
– reference: Wu S, Zou MH (2020) AMPK, mitochondrial function, and cardiovascular disease [J]. Int J Mol Sci 21(14):4987
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Snippet Parkinson’s disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a...
Parkinson's disease (PD) is a neurodegenerative disease that mainly manifests as cognitive decline and motor dysfunction, the treatment of which is still a...
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SubjectTerms Acupuncture
AMP-Activated Protein Kinases
Animal tissues
Animals
Apoptosis
Biomedical and Life Sciences
Biomedicine
Calcium (mitochondrial)
Calcium ions
Cell Biology
Chorea
Cognitive ability
Damage
Disease Models, Animal
Disease resistance
Electroacupuncture
Flow cytometry
Health services
Immunofluorescence
Immunohistochemistry
Inflammation
Inflammatory response
Male
Membrane potential
Mice
Mice, Inbred C57BL
Mitochondria
Mitochondrial Diseases
Movement disorders
MPTP
Neurochemistry
Neurodegenerative Diseases
Neurology
Neurosciences
Oxidative stress
Parkinson Disease - therapy
Parkinson's disease
Proteomics
Signal transduction
SIRT1 protein
Sirtuin 1 - genetics
Substantia nigra
Western blotting
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Title Electroacupuncture Improves Neuronal Damage and Mitochondrial Dysfunction Through the TRPC1 and SIRT1/AMPK Signaling Pathways to Alleviate Parkinson’s Disease in Mice
URI https://link.springer.com/article/10.1007/s12031-023-02186-z
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