Dihydromyricetin Improves Endothelial Dysfunction in Diabetic Mice via Oxidative Stress Inhibition in a SIRT3-Dependent Manner

Hua, Yuyun; Zhang, Yue; Gong, Weiwei; Ding, Yue; Shen, Jieru; Li, Hua; Chen, Yun

doi:10.3390/ijms21186699

Cited by 30 publications

(16 citation statements)

References 60 publications

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“…Several data has proved the protective effects of DHM against vascular function impairment; DHM ameliorated the diabetic induced vascular dysfunction as well as inhibited the development of atherosclerosis via attenuation of endothelial cell activation and damage. These beneficial vascular effects of DHM were found to be mediated via attenuation of ROS release [33][34][35][36]. Also, DHM was found to attenuate vascular iNOS/NO expression while enhances eNOS production leading to improved vascular activity [37,38].…”

Section: Discussionmentioning

confidence: 90%

Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Anter

Awad

Kamed

et al. 2023

Journal of advanced Biomedical and Pharmaceutical Sciences

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Gentamicin causes an impairment of vascular function due to endothelial cell damage. Renal injury by gentamicin may contribute to the development of vascular dysfunction due to decreased NO bioavailability as well as increased oxidative stress and inflammation. In this study we investigate the role of DHM on vascular dysfunction induced by gentamicin. Male Wistar rats were divided into 3 groups (n= 6, each); control group; received the vehicle, gentamicin group; given gentamicin (100 mg/kg/day i.p) for 8 days and gentamicin + dihydromyricetin group; rats were treated with dihydromyricetin (200 mg/kg, p.o) concurrently with gentamicin. DHM reversed the GTN-induced histopathological changes of aortic rings. In addition, administration of DHM to GTN treated rats improved the vascular functions evident as enhanced vasorelaxation and vasoconstriction responses to acetylcholine and phenylephrine, respectively. Further, DHM increased the vascular levels of GSH and total antioxidant activity. Immunohistochemical analysis of aortic sections revealed that DHM treatment downregulated NF-κB, TNF-α and caspase-3 expression. Our data provide a new evidence for the protective effects of DHM against gentamicin-induced vascular dysfunction via provoking antioxidant, anti-inflammatory and antiapoptotic effects.

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Section: Discussionmentioning

confidence: 90%

Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Anter

Awad

Kamed

et al. 2023

Journal of advanced Biomedical and Pharmaceutical Sciences

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“…CAT protects cells from H 2 O 2 toxicity by participating in a biodefense system [37]. Hua et al showed that DHM improved endothelial dysfunction in diabetic mice via oxidative stress inhibition in a SIRT3-dependent manner [38]. Zhang et al showed that DHM protected HUVECs from oxidative damage induced by sodium nitroprusside by activating the PI3K/Akt/FoxO3a signaling pathway [39].…”

Section: Discussionmentioning

confidence: 99%

Dihydromyricetin Enhances Intestinal Antioxidant Capacity of Growing-Finishing Pigs by Activating ERK/Nrf2/HO-1 Signaling Pathway

Wei

Chen

et al. 2022

Antioxidants

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Oxidative stress is one of the main factors affecting animal health and reducing performance. The small intestine is the primary site of free-radical attacks. Dihydromyricetin (DHM) is a flavonoid compound with antioxidant, anti-inflammatory, and other biological activities, which is mainly extracted from Rattan tea. However, the effects of DHM on the intestinal antioxidant function of growing-finishing pigs and related mechanisms remain unclear. The aim of this study was to investigate the effect of dietary DHM supplementation on the intestinal antioxidant capacity of growing-finishing pigs and its mechanism. Our results show that dietary 0.03% DHM increased the activities of the total antioxidant capacity (T-AOC), catalase (CAT), and glutathione peroxidase (GSH-Px), decreased malondialdehyde (MDA) level, and upregulated protein expressions of HO-1, NQO1, nuclear Nrf2, and phospho-ERK (p-ERK) in the jejunum of growing-finishing pigs. Again, we found that 20 μmol/mL and 40 μmol/mL DHM treatment significantly upregulated the protein expression of HO-1 and promoted the nuclear translocation of Nrf2 and ERK phosphorylation in IPCE-J2 cells. ERK inhibitor PD98059 eliminated the DHM-induced upregulation of p-ERK, nuclear Nrf2, and HO-1. Our findings provided the first evidence that DHM enhanced the intestinal antioxidant capacity of growing-finishing pigs by activating the ERK/Nrf2/HO-1 signaling pathway.

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“…DHM can regulate the expression of target genes induced by TNF-α by suppressing NF-κB activation. 18 Thus, we explored whether DHM could suppress the inflammation and oxidative stress in the liver induced by APAP and the corresponding molecular mechanism.…”

Section: Discussionmentioning

confidence: 99%

Evaluation on Hepatoprotection of Dihydromyricetin in Acetaminophen-Induced Hepatotoxicity Based on Analysis of Inflammation and Apoptosis Mediated by PI3K/AKT Pathway

Gong

Zhang

et al. 2022

Natural Product Communications

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Purpose: We aimed to investigate whether dihydromyricetin (DHM) could alleviate acetaminophen (APAP)-induced liver damage in mice, and to verify whether the process is associated with the PI3K/AKT signaling pathway. Methods: The contents of DHM in serum and related physiological indicators in blood and liver tissue were measured, respectively. We used haematoxylin and eosin (H&E), TUNEL, Hoechst 33,258, immunofluorescence assay and western blot methods to comprehensively assess the protective mechanism and therapeutic effect of DHM on liver damage induced by APAP (250 mg/kg) in mice. Results: APAP (250 mg/kg) could increase the expression of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α), and interleukin 1β (IL-1β) and cause 4-hydroxy-2-nonenal (4-HNE) and Cytochrome P450 2E1 (CYP2E1) overexpression and stress response in the PI3K/AKT pathway. DHM was also detected in the serum of mice about five minutes after administration. DHM pretreatment could reverse GSH depletion and CYP2E1 overexpression, reduce the expression of ALT, AST, malondialdehyde, 4-HNE, TNF-α, and IL-1β, meanwhile it could reverse the abnormal expression of PI3K/AKT signaling pathway-related proteins which were induced by APAP. DHM pretreatment significantly reduced APAP-induced liver tissue apoptosis, necrosis, and inflammatory infiltration. Conclusion: DHM had a hepatoprotective effect on hepatotoxicity induced by APAP, which was shown by inhibiting oxidative stress and inflammatory responses, and reducing hepatocyte apoptosis by activating the PI3K/AKT signaling pathway.

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Dihydromyricetin Improves Endothelial Dysfunction in Diabetic Mice via Oxidative Stress Inhibition in a SIRT3-Dependent Manner

Cited by 30 publications

References 60 publications

Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Dihydromyricetin Enhances Intestinal Antioxidant Capacity of Growing-Finishing Pigs by Activating ERK/Nrf2/HO-1 Signaling Pathway

Evaluation on Hepatoprotection of Dihydromyricetin in Acetaminophen-Induced Hepatotoxicity Based on Analysis of Inflammation and Apoptosis Mediated by PI3K/AKT Pathway

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