α-Bisabolol and royal jelly differentially mitigate thioacetamide-induced hepatic fibrosis in rats associated with the inhibition of TGF-β1/FAK/α-SMA signaling.

Hepatic fibrosis is a global health burden that accounts for high mortality. No definitive therapy to suppress the fibrosis so far. Thus, looking for an effective remedy to address the unmet medical need is crucial. We aimed to scrutinize the efficacy of royal jelly (RJ) and/or α-Bisabolol (BISA) in the regression of fibrosis provoked by thioacetamide (TAA), focusing on their action on redox status, NF-κBp65, apoptosis, and TGF-β1/FAK/α-SMA pathway. TAA was injected intraperitoneally twice weekly to trigger hepatic fibrosis. Rats were gavaged with RJ (100 mg/kg) and/or BISA (50 mg/kg) daily for 8 weeks. The findings elucidated that RJ and/or BISA alleviated TAA-provoked fibrosis mirrored by the improvement of hepatotoxicity serum indices, abolishing oxidative stress, and repair the morphological alterations. Additionally, RJ and BISA suppressed the hepatic inflammation induced by TAA through downregulating NF-κBp65 expression, reducing TNF-α and IL-6 concentrations, and elevating IL-10 level. Their anti-fibrotic effect was emphasized from the decline in FAK, Smad3, COL-III, hydroxyproline levels, and TGF-β1, α-SMA immunoexpression. BISA displayed better ameliorative action than RJ. Conclusively, RJ and/or BISA possess a hepatoprotective activity against TAA-mediated fibrosis by enhancing antioxidant defense, inhibiting NF-κBp65, and modulating TGF-β1/FAK/α-SMA signaling. RJ and BISA might be prospective candidates to combat hepatic fibrosis.