Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation | ||||
| Journal of advanced Biomedical and Pharmaceutical Sciences | ||||
| Article 7, Volume 6, Issue 2, April 2023, Page 107-113 PDF (729.03 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/jabps.2023.194992.1181 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Aliaa Anter; Eman M. Awad; Amr A. Kamel; Asmaa I. Matouk 
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| Department of Pharmacology & Toxicology, Faculty of Pharmacy, Minia University, 61519 El-Minia, Egypt | ||||
| Abstract | ||||
| 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, antiinflammatory and antiapoptotic effects. | ||||
| Keywords | ||||
| DHM; Vascular; Nitric oxide; TNF-α; aorta | ||||
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