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

Objective: (CD) on dexamethasone (DEX)-induced hepatic injuries were investigated. Materials and Methods: studies were performed in HepG2 cells that grouped as: Control, DEX (1 µM), DEX+CD (0.1, 0.5 and 1 mg/ml), CD 0.5 mg/ml, and DEX+MET (500 µM). Cell viability and animal weight changes were recorded. Following the study period, biochemical and histopathological analyses were conducted on hepatic tissue and HepG2 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<0.05) reduced in both models. Moreover, the DEX-induced oxidative stress was improved by CD extract (45%). The DEX-elevated blood glucose (20%) and triglycerides (60%) were reduced in CD-treated animals. The DEX-generated hepatic macrovesicles and lipid droplets in HepG2 cells were reduced. Conclusion: These results suggest that CD extract could be an effective compound for protection from DEX-induced hepatic injuries.