Resveratrol mitigates pancreatic TF activation and autophagy-mediated beta cell death via inhibition of CXCL16/ox-LDL pathway: A novel protective mechanism against type 1 diabetes mellitus in mice

The role of CXC chemokine ligand 16 (CXCL16), oxidized LDL (ox-LDL), tissue factor (TF) and autophagy-induced beta cell death in type 1 diabetes mellitus (T1DM) pathogenesis is still unclear. We examined the therapeutic potential and mechanism of resveratrol (RES) against T1DM. Diabetes was induced...

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Published inEuropean journal of pharmacology Vol. 901; p. 174059
Main Authors Darwish, Mostafa A., Abdel-Bakky, Mohamed S., Messiha, Basim A.S., Abo-Saif, Ali A., Abo-Youssef, Amira M.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 15.06.2021
Subjects
Animals
Antioxidants - pharmacology
Autophagy - drug effects
Cell Death - drug effects
Chemokine CXCL16 - drug effects
CXCL16
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - prevention & control
Diabetes Mellitus, Type 1 - prevention & control
Glucose Tolerance Test
Insulin-Secreting Cells - drug effects
Lipoproteins, LDL - drug effects
Male
Mice
Mice, Inbred BALB C
Ox-LDL
Protective Agents - pharmacology
Protective Agents - therapeutic use
Resveratrol
Resveratrol - pharmacology
Signal Transduction - drug effects
Thromboplastin - metabolism
Type 1 diabetes
TF
Type 1 diabetes
Resveratrol
CXCL16
Ox-LDL
Online AccessGet full text

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Abstract The role of CXC chemokine ligand 16 (CXCL16), oxidized LDL (ox-LDL), tissue factor (TF) and autophagy-induced beta cell death in type 1 diabetes mellitus (T1DM) pathogenesis is still unclear. We examined the therapeutic potential and mechanism of resveratrol (RES) against T1DM. Diabetes was induced in Balb/c mice by i. p. injection of 55 mg/kg streptozotocin (STZ) for five consecutive days. The control group received vehicles. RES or (RES + STZ) groups received RES (50 mg/kg, i. p.) daily for 12 days starting from the fourth day of buffer or STZ injections, respectively. Blood glucose, serum insulin, beta cell mass, serum lipid profiles, histological changes, oxidative stress biomarkers were determined. Moreover, CXCL16, TF, ox-LDL, P62 and LC3 tissue expression were also analyzed. Diabetic mice showed a marked deterioration in biochemical, physical and oxidative stress parameters. Interestingly, immunofluorescence analysis showed a remarkable elevation in CXCL16 (12 folds), ox-LDL (9 folds), TF (8.3 folds) in pancreatic B-cells. Moreover, western blotting revealed a profound increase in ox-LDL (2.6 folds), TF (3.2 folds), while a significant decline in P62 (0.34) and LC3 (0.25) when compared to control. RES mitigated biochemical, physical, oxidative imbalance and distorted pancreatic architecture in T1DM mice. Intriguingly, CXCL16, ox-LDL, TF and autophagic markers were also restored after RES treatment. Our data give the first direct evidence that beta cell–specific CXCL16/ox-LDL pathway activation is a potential trigger of TF activation and autophagic beta cell death in T1DM. Moreover, RES may have potential therapeutic applications for prevention of T1DM mainly via ameliorating this pathway.
AbstractList The role of CXC chemokine ligand 16 (CXCL16), oxidized LDL (ox-LDL), tissue factor (TF) and autophagy-induced beta cell death in type 1 diabetes mellitus (T1DM) pathogenesis is still unclear. We examined the therapeutic potential and mechanism of resveratrol (RES) against T1DM. Diabetes was induced in Balb/c mice by i. p. injection of 55 mg/kg streptozotocin (STZ) for five consecutive days. The control group received vehicles. RES or (RES + STZ) groups received RES (50 mg/kg, i. p.) daily for 12 days starting from the fourth day of buffer or STZ injections, respectively. Blood glucose, serum insulin, beta cell mass, serum lipid profiles, histological changes, oxidative stress biomarkers were determined. Moreover, CXCL16, TF, ox-LDL, P62 and LC3 tissue expression were also analyzed. Diabetic mice showed a marked deterioration in biochemical, physical and oxidative stress parameters. Interestingly, immunofluorescence analysis showed a remarkable elevation in CXCL16 (12 folds), ox-LDL (9 folds), TF (8.3 folds) in pancreatic B-cells. Moreover, western blotting revealed a profound increase in ox-LDL (2.6 folds), TF (3.2 folds), while a significant decline in P62 (0.34) and LC3 (0.25) when compared to control. RES mitigated biochemical, physical, oxidative imbalance and distorted pancreatic architecture in T1DM mice. Intriguingly, CXCL16, ox-LDL, TF and autophagic markers were also restored after RES treatment. Our data give the first direct evidence that beta cell-specific CXCL16/ox-LDL pathway activation is a potential trigger of TF activation and autophagic beta cell death in T1DM. Moreover, RES may have potential therapeutic applications for prevention of T1DM mainly via ameliorating this pathway.
ArticleNumber 174059
Author Abdel-Bakky, Mohamed S.
Abo-Youssef, Amira M.
Abo-Saif, Ali A.
Messiha, Basim A.S.
Darwish, Mostafa A.
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Keywords TF
Type 1 diabetes
Resveratrol
CXCL16
Ox-LDL
Language English
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SSID ssj0005925
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Snippet The role of CXC chemokine ligand 16 (CXCL16), oxidized LDL (ox-LDL), tissue factor (TF) and autophagy-induced beta cell death in type 1 diabetes mellitus...
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pubmed
elsevier
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StartPage 174059
SubjectTerms Animals
Antioxidants - pharmacology
Autophagy - drug effects
Cell Death - drug effects
Chemokine CXCL16 - drug effects
CXCL16
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - prevention & control
Diabetes Mellitus, Type 1 - prevention & control
Glucose Tolerance Test
Insulin-Secreting Cells - drug effects
Lipoproteins, LDL - drug effects
Male
Mice
Mice, Inbred BALB C
Ox-LDL
Protective Agents - pharmacology
Protective Agents - therapeutic use
Resveratrol
Resveratrol - pharmacology
Signal Transduction - drug effects
Thromboplastin - metabolism
Type 1 diabetes
Title Resveratrol mitigates pancreatic TF activation and autophagy-mediated beta cell death via inhibition of CXCL16/ox-LDL pathway: A novel protective mechanism against type 1 diabetes mellitus in mice
URI https://dx.doi.org/10.1016/j.ejphar.2021.174059
https://www.ncbi.nlm.nih.gov/pubmed/33794215
Volume 901
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