Steroids · 2026
The protective effects of luteolin and oleuropein against dexamethasone-induced hyperlipidemia.
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Aziz Lourin Nasr, Mahmoud Mohamed Omar, Ibrahim Ibrahim Taha
Аннотация
BACKGROUND: Dexamethasone-induced hyperlipidemia is a well-documented metabolic complication associated with prolonged glucocorticoid therapy. The present study aims to investigate the potential protective effects of the selected natural antioxidants luteolin and oleuropein against dexamethasone-induced hyperlipidemia.
METHODOLOGY: The study was conducted on five groups of female Wistar rats, including a normal control group, a dexamethasone-induced hyperlipidemia group, and three treatment groups. The treatment groups consisted of dexamethasone-administered rats receiving luteolin or oleuropein (100 mg/kg BW) individually or in combination (luteolin + oleuropein) for a duration of one month.
RESULTS: Dexamethasone induced hyperlipidemia, hepatic injury, and oxidative stress, as evidenced by increased levels of aspartate aminotransferase (AST; +154%), alanine aminotransferase (ALT; +121%), total cholesterol (TC; +75%), triglycerides (+132%), and malondialdehyde (+85%), while reducing catalase and glutathione by approximately 50.5% and 62%, respectively, compared with the control group. Treatment with either luteolin or oleuropein individually mitigated these changes (AST: -47.0% and - 46.4%; ALT: -37.2% and - 36.4%; TC: -34.8% and - 33.1%; triglycerides: -41.7% and - 40.5%; malondialdehyde: -28.4% and - 26.0%; catalase: +79.2% and + 74.8%; and glutathione: +104.8% and + 102.3%, respectively). Combined treatment provided the greatest protection, and histological examination revealed partial restoration of normal hepatic architecture.
CONCLUSION: The study suggests that luteolin and oleuropein help counteract dexamethasone-induced hyperlipidemia. Their administration reduced oxidative stress and liver enzyme levels (AST, ALT, and ALP) and improved lipid profiles, indicating their potential as therapeutic agents against glucocorticoid-related metabolic disturbances. The enhanced effectiveness observed in the combined treatment groups likely reflects synergistic activity between these compounds.
METHODOLOGY: The study was conducted on five groups of female Wistar rats, including a normal control group, a dexamethasone-induced hyperlipidemia group, and three treatment groups. The treatment groups consisted of dexamethasone-administered rats receiving luteolin or oleuropein (100 mg/kg BW) individually or in combination (luteolin + oleuropein) for a duration of one month.
RESULTS: Dexamethasone induced hyperlipidemia, hepatic injury, and oxidative stress, as evidenced by increased levels of aspartate aminotransferase (AST; +154%), alanine aminotransferase (ALT; +121%), total cholesterol (TC; +75%), triglycerides (+132%), and malondialdehyde (+85%), while reducing catalase and glutathione by approximately 50.5% and 62%, respectively, compared with the control group. Treatment with either luteolin or oleuropein individually mitigated these changes (AST: -47.0% and - 46.4%; ALT: -37.2% and - 36.4%; TC: -34.8% and - 33.1%; triglycerides: -41.7% and - 40.5%; malondialdehyde: -28.4% and - 26.0%; catalase: +79.2% and + 74.8%; and glutathione: +104.8% and + 102.3%, respectively). Combined treatment provided the greatest protection, and histological examination revealed partial restoration of normal hepatic architecture.
CONCLUSION: The study suggests that luteolin and oleuropein help counteract dexamethasone-induced hyperlipidemia. Their administration reduced oxidative stress and liver enzyme levels (AST, ALT, and ALP) and improved lipid profiles, indicating their potential as therapeutic agents against glucocorticoid-related metabolic disturbances. The enhanced effectiveness observed in the combined treatment groups likely reflects synergistic activity between these compounds.