Journal of ethnopharmacology · 2025
Hepatoprotective potential of Diospyros melanoxylon (Roxb.) leaf extract by inhibition of IL-6, COX-2, and 5-LOX expression in paracetamol intoxicated rats.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Babu Sucharita, Kar Biswakanth, Kumar Santosh, Pattnaik Gurudutta, Kulkarni Sharvari, Pattanaik Sovan, Nanda Ashirbad, Das Chandan, Dash Priyanka, Rai Vineet Kumar, Halder Jitu, Ghosh Goutam, Rath Goutam
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Diospyros melanoxylon, Roxb., (Ebenaceae), native to South and Southeast Asia, has been traditionally used to treat liver disorders, jaundice, tuberculosis, and chronic wounds and inflammatory conditions.
AIM OF THE STUDY: To evaluate the hepatoprotective effect of D. melanoxylon leaf methanolic extract (MDML) in paracetamol (PCM)-induced liver toxicity in rats.
MATERIAL AND METHOD: Phytoconstituents in the MDML were identified via LC-MS. Molecular docking and dynamics simulations evaluated the binding stability of ursolic acid (UA) with IL-6, COX-2, and LOX. In vitro COX-2 and 5-LOX inhibition assays assessed anti-inflammatory potential. Hepatoprotective efficacy was examined in PCM-intoxicated rats treated with MDML (200, 300, 400 mg/kg). Biochemical markers, serum enzymes (ALT, AST, ALP, GGT, LDH), protein profile (TP, ALB, GLB, TB), antioxidant enzymes (SOD, CAT, GSH), oxidative stress marker (MDA), and cytokines (IL-6, IL-10, IL-1β, TNF-α) were analyzed. Histopathological examination of liver tissues further validated the findings.
RESULT: Nineteen compounds were identified by LC-MS. UA showed strong docking affinities with IL-6 (-7.0 kcal/mol), COX-2 (-8.5 kcal/mol), and LOX, with MD simulations confirming stable interactions. MDML (400 μg/mL) inhibited COX-2 and 5-LOX by 78.45 % and 85.45 %, respectively. In vivo, MDML (400 mg/kg) significantly (p < 0.01, p < 0.001) reduced liver enzymes and oxidative stress markers, while improving antioxidant levels and cytokine balance. Significant reductions in TB and GLB, with corresponding increases in TP and TLB, were observed. Histology revealed dose-dependent restoration of hepatic architecture comparable to controls.
CONCLUSION: MDML shows dose-dependent hepatoprotection against PCM-induced toxicity, likely due to the presence of UA, supporting its traditional use in liver disorders.
AIM OF THE STUDY: To evaluate the hepatoprotective effect of D. melanoxylon leaf methanolic extract (MDML) in paracetamol (PCM)-induced liver toxicity in rats.
MATERIAL AND METHOD: Phytoconstituents in the MDML were identified via LC-MS. Molecular docking and dynamics simulations evaluated the binding stability of ursolic acid (UA) with IL-6, COX-2, and LOX. In vitro COX-2 and 5-LOX inhibition assays assessed anti-inflammatory potential. Hepatoprotective efficacy was examined in PCM-intoxicated rats treated with MDML (200, 300, 400 mg/kg). Biochemical markers, serum enzymes (ALT, AST, ALP, GGT, LDH), protein profile (TP, ALB, GLB, TB), antioxidant enzymes (SOD, CAT, GSH), oxidative stress marker (MDA), and cytokines (IL-6, IL-10, IL-1β, TNF-α) were analyzed. Histopathological examination of liver tissues further validated the findings.
RESULT: Nineteen compounds were identified by LC-MS. UA showed strong docking affinities with IL-6 (-7.0 kcal/mol), COX-2 (-8.5 kcal/mol), and LOX, with MD simulations confirming stable interactions. MDML (400 μg/mL) inhibited COX-2 and 5-LOX by 78.45 % and 85.45 %, respectively. In vivo, MDML (400 mg/kg) significantly (p < 0.01, p < 0.001) reduced liver enzymes and oxidative stress markers, while improving antioxidant levels and cytokine balance. Significant reductions in TB and GLB, with corresponding increases in TP and TLB, were observed. Histology revealed dose-dependent restoration of hepatic architecture comparable to controls.
CONCLUSION: MDML shows dose-dependent hepatoprotection against PCM-induced toxicity, likely due to the presence of UA, supporting its traditional use in liver disorders.