Neuroprotectant Effects of Hibiscetin in 3-Nitropropionic Acid-Induced Huntington's Disease via Subsiding Oxidative Stress and Modulating Monoamine Neurotransmitters in Rats Brain
Previously reported data suggest that hibiscetin, isolated from , contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against...
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| Published in | Molecules (Basel, Switzerland) Vol. 28; no. 3; p. 1402 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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01.02.2023
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| Abstract | Previously reported data suggest that hibiscetin, isolated from
, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD).
To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups (
= 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated.
The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin.
The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models. |
|---|---|
| AbstractList | Previously reported data suggest that hibiscetin, isolated from
, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD).
To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups (
= 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated.
The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin.
The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models. Previously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD).BACKGROUNDPreviously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington's disease (HD).To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups (n = 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated.METHODSTo investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups (n = 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated.The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin.RESULTSThe hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin.The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models.CONCLUSIONThe current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models. Background: Previously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington’s disease (HD). Methods: To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups (n = 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated. Results: The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin. Conclusion: The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models. Background: Previously reported data suggest that hibiscetin, isolated from roselle , contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington’s disease (HD). Methods: To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats were divided into four groups ( n = 6); (group-1) treated with normal saline, (group-2) hibiscetin (10 mg/kg) only, (group-3) 3-NPA only, and (group-4) 3-NPA +10 mg/kg hibiscetin. The efficacy of hibiscetin 10 mg/kg was studied with the administration of 3-NPA doses for the induction of experimentally induced HD symptoms in rats. The mean body weight (MBW) was recorded at end of the study on day 22 to evaluate any change in mean body weight. Several biochemical parameters were assessed to support oxidative stress (GSH, SOD, CAT, LPO, GR, and GPx), alteration in neurotransmitters (DOPAC, HVA, 5-HIAA, norepinephrine, serotonin, GABA, and dopamine), alterations in BDNF and cleaved caspase (caspase 3) activity. Additionally, inflammatory markers, i.e., tumor necrosis factor alpha (TNF-α), interleukins beta (IL-1β), and myeloperoxidase (MPO) were evaluated. Results: The hibiscetin-treated group exhibits a substantial restoration of MBW than the 3-NPA control group. Furthermore, 3-NPA caused a substantial alteration in biochemical, neurotransmitter monoamines, and neuroinflammatory parameters which were restored successfully by hibiscetin. Conclusion: The current study linked the possible role of hibiscetin by offering neuroprotection in experimental animal models. |
| Audience | Academic |
| Author | Sayyed, Nadeem Hajjar, Baraa Mohammed Kazmi, Imran Almaniea, Mohammad A Mahdi, Wael A Al-Abbasi, Fahad A Alshehri, Sultan AlGhamdi, Shareefa A Alghamdi, Amira M Imam, Syed Sarim |
| AuthorAffiliation | 2 Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia 3 Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia 4 School of Pharmacy, Glocal University, Saharanpur 247121, India 1 Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia |
| AuthorAffiliation_xml | – name: 1 Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia – name: 3 Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia – name: 4 School of Pharmacy, Glocal University, Saharanpur 247121, India – name: 2 Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia |
| Author_xml | – sequence: 1 givenname: Wael A orcidid: 0000-0002-7083-1753 surname: Mahdi fullname: Mahdi, Wael A organization: Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia – sequence: 2 givenname: Shareefa A orcidid: 0000-0002-6603-6116 surname: AlGhamdi fullname: AlGhamdi, Shareefa A organization: Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia – sequence: 3 givenname: Amira M surname: Alghamdi fullname: Alghamdi, Amira M organization: Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia – sequence: 4 givenname: Syed Sarim orcidid: 0000-0002-8913-0826 surname: Imam fullname: Imam, Syed Sarim organization: Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia – sequence: 5 givenname: Sultan orcidid: 0000-0002-0922-9819 surname: Alshehri fullname: Alshehri, Sultan organization: Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia – sequence: 6 givenname: Mohammad A surname: Almaniea fullname: Almaniea, Mohammad A organization: Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia – sequence: 7 givenname: Baraa Mohammed surname: Hajjar fullname: Hajjar, Baraa Mohammed organization: Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia – sequence: 8 givenname: Fahad A surname: Al-Abbasi fullname: Al-Abbasi, Fahad A organization: Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia – sequence: 9 givenname: Nadeem surname: Sayyed fullname: Sayyed, Nadeem organization: School of Pharmacy, Glocal University, Saharanpur 247121, India – sequence: 10 givenname: Imran orcidid: 0000-0003-1881-5219 surname: Kazmi fullname: Kazmi, Imran organization: Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36771072$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3390_biomedicines12030625 crossref_primary_10_1007_s43440_024_00619_z crossref_primary_10_1016_j_chphi_2023_100416 crossref_primary_10_1371_journal_pone_0293660 crossref_primary_10_1007_s11064_024_04158_0 crossref_primary_10_7717_peerj_16795 |
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| Snippet | Previously reported data suggest that hibiscetin, isolated from
, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and... Background: Previously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including... Previously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including... Background: Previously reported data suggest that hibiscetin, isolated from roselle , contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including... |
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| SubjectTerms | 3-Nitropropionic acid Acute toxicity Animal cognition Animal models Animals Body Weight Brain Brain research Brain-derived neurotrophic factor Care and treatment Caspase-3 Disease Dopamine Evaluation Flavonoids Health aspects hibiscetin Huntington Disease - chemically induced Huntington Disease - drug therapy Huntington's chorea Huntington's disease Huntingtons disease Inflammation Monoamines Neurodegeneration Neurons Neuroprotection Neuroprotective agents Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Neurotransmitter Agents - pharmacology Neurotransmitters Nitro Compounds - pharmacology Norepinephrine Oxidative Stress Peroxidase Pharmacology, Experimental Physiological effects Phytochemicals Propionates - pharmacology Proteins Rats Rats, Wistar Serotonin Signs and symptoms Toxicity Tumor necrosis factor-TNF Tumor necrosis factor-α γ-Aminobutyric acid |
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| Title | Neuroprotectant Effects of Hibiscetin in 3-Nitropropionic Acid-Induced Huntington's Disease via Subsiding Oxidative Stress and Modulating Monoamine Neurotransmitters in Rats Brain |
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