Taxifolin, a novel food, attenuates acute alcohol-induced liver injury in mice through regulating the NF-κB-mediated inflammation and PI3K/Akt signalling pathways

Abstract

Context: Taxifolin (TAX) has effective anti-inflammatory, antioxidant and hepatoprotective activities, but its potential mechanism has not been revealed. Objective: To evaluate the potential protective effect of TAX on acute alcohol-induced liver injury in mice. Materials and methods: Alcoholic liver injury model was established by oral alcohol in mice, and randomly distributed in five groups (n ¼ 10): Normal group (oral saline only); Alcohol group (concentration of fermented alcohol: 56%, 6 mL/kg); TAX groups, mice were orally administered with alcohol, and then TAX with doses of 20, 40, 80 mg/kg, respectively. Oral administration was conducted for 6 weeks. Results: TAX treatment illustrated that the level of alanine aminotransferase (ALT) was reduced to 65.90 ± 2.26 U/L and aspartate aminotransferase (AST) to 33.28 ± 5.62 U/L compared with alcohol group (ALT 124.51 ± 4.40 U/L, AST 61.70 ± 4.09 U/L), while superoxide dismutase (SOD) was increased to 49.81 ± 2.39 U/mg and glutathione (GSH) to 8.16 ± 0.44 lmol/g, but MDA was reversed to 2.53 ± 0.24 nmol/ mg. Histopathological examination showed TAX treatment alleviated alcohol-induced hepatocyte necrosis and inflammatory infiltration. Meanwhile, Western blot and rt-PCR indicated TAX reduced IL-6 to 2.49 ± 0.25 pg/mL and TNF-a to 1.79 ± 0.20 pg/mL, and inhibiting NF-jB activation in liver. Moreover, TAX reversed alcohol-induced apoptosis by regulating the expression of PI3K/Akt and its downstream apoptotic factors. Conclusions:The research provides novel evidence of the hepatoprotective effect of TAX on alcoholinduced liver injury, while also providing the possibility for future treatment of alcoholic liver disease.

Renoprotective and Oxidative Stress-Modulating Effects of Taxifolin against Cadmium-Induced Nephrotoxicity in Mice

“…An additional advantage of TA therapy for Cd-intoxicated patients is supported by the research that shows it might diminish inflammation and/or suppress cytokine storms in those individuals exposed to Cd. Furthermore, a recent study demonstrated that TA showed hepatoprotective effects against alcohol-induced hepatic damage via modulating the NF-κB-mediated pro-inflammatory cytokines production and hepatic inflammation [ 21 ].…”

“…TA has also been shown to prevent OS-stimulated retinal pigment epithelium (RPE) cell destruction and apoptosis via activation of Nrf2 and the phase II antioxidant enzyme system. Furthermore, TA ameliorated acute alcohol-stimulated hepatic damage via modulating the NF-κB-mediated inflammation in mice [ 21 ].…”

Dihydromyricetin Reverses Thioacetamide-Induced Liver Fibrosis Through Inhibiting NF-κB-Mediated Inflammation and TGF-β1-Regulated of PI3K/Akt Signaling Pathway

“…The levels of GSH, MDA, and SOD are important indicators reflecting oxidative stress damage ( Ding et al, 2021 ). Therefore, the levels of GSH, MDA and SOD in liver tissue were detected.…”

Licochalcone B Induced Apoptosis and Autophagy in Osteosarcoma Tumor Cells <i>via</i> the Inactivation of PI3K/AKT/mTOR Pathway

“…[21][22][23] According to previous research, PI3K signaling is involved in a variety of human disorders, such as proliferative disorders and cancers. 6,29,30) Furthermore, the PI3K/AKT/mTOR pathway has been shown to modulate tumor cell autophagy and apoptosis. 31) As a result, inhibiting PI3K signaling has been identified as a potential treatment alternative for these disorders, and PI3K serves as a major target for drug development.…”