Dexamethasone-induced hepatic biochemical and pathological damages are attenuated by Cynodon dactylon extract containing hexadecanoic acid via reduction of glucose uptake: In vitro and in vivo studies

Objective: The protective effects of ethanolic extract of Cynodon dactylon (CD) on dexamethasone (DEX)-induced hepatic injuries were investigated.Materials and Methods: Following GC-MS phytochemical analyses of the extract, in vivo studies were conducted in male rats which were grouped as: control, dexamethasone (۸mg/kg, intraperitoneally), DEX+CD (۱۰۰, ۲۰۰ and ۴۰۰ mg/kg, orally), CD ۴۰۰ and DEX+metformin (MET, ۳۰۰mg/kg, orally) for ۱۵ days. The in vitro studies were performed in HepG۲ cells that grouped as: Control, DEX (۱ µM), DEX+CD (۰.۱, ۰.۵ and ۱ mg/ml), CD ۰.۵ mg/ml, and DEX+MET (۵۰۰ µM). Cell viability and animal weight changes were recorded. Following the study period, biochemical and histopathological analyses were conducted on hepatic tissue and HepG۲ cells.Results: Findings revealed that CD extract does have concentration-dependent free radical-scavenging activity, and it possesses phenols and flavonoids contents. The most abundant compound of the CD extract was n-hexadecanoic acid. The DEX-induced hepatic functional enzymes and lactate dehydrogenase levels were significantly (p<۰.۰۵) reduced in both models. Moreover, the DEX-induced oxidative stress was improved by CD extract (۴۵%). The DEX-elevated blood glucose (۲۰%) and triglycerides (۶۰%) were reduced in CD-treated animals. The DEX-generated hepatic macrovesicles and lipid droplets in HepG۲ cells were reduced.Conclusion: These results suggest that CD extract could be an effective compound for protection from DEX-induced hepatic injuries.

کلیدواژه ها:

Dexamethasone ، Hepatic injuries ، Hypolipidemic effect ، glucose uptake