Liver fibrosis is a progressive pathological condition that may lead to cirrhosis. Moringa oleifera (MO) has antifibrotic potential, while quercetin (Q) and kaempferol (K), its major flavonoids, also exhibit antioxidant, anti-inflammatory, and antifibrotic activities capable of promoting fibrosis regression. Direct comparative evidence on the antifibrotic effects of MO extract and its major flavonoids remains limited. This study compared the antifibrotic effects of MO extract, Q, K, and KQ in a rat model of liver fibrosis and evaluated miR-29b expression as an antifibrotic microRNA marker. Thirty male Wistar rats were divided into six groups, and fibrosis was induced with 10% CCl4 for 11 weeks. The model (M) group was euthanized after induction, while the remaining groups received 6 weeks of treatment with MO (600 mg/kg/day), Q (15 mg/kg/day), K (12.5 mg/kg/day), KQ (K 12.5 mg/kg/day + Q 15 mg/kg/day), or placebo (P; aquadest 2.5 mL). Fibrosis score (Metavir), liver histology (Masson’s Trichrome and hematoxylin–eosin staining), serum AST/ALT levels, and hepatic miR-29b expression (measured by RT-PCR) were analyzed. METAVIR scoring showed advanced fibrosis in the M and P groups, with significantly reduced fibrosis severity in the MO and K groups compared with the M group (P < 0.05). Hepatic miR-29b expression was significantly upregulated in MO, KQ, K and placebo groups (P < 0.01). This study showed that MO and K exert significant antifibrotic effects in promoting regression of liver fibrosis, while miR-29b upregulation may support their antifibrotic activity.
Supriono et al. (Sun,) studied this question.