Aloin Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury via Inhibiting TLR4/MyD88/NF-κB Signal Pathway In Vivo and In Vitro.
Yi-Chao DuBaolin QianLin GaoPeng TanHao ChenAnkang WangTianxiang ZhengShilin PuXianming XiaWen-Guang FuPublished in: Oxidative medicine and cellular longevity (2019)
We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response. Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).
Keyphrases
- toll like receptor
- inflammatory response
- nuclear factor
- oxidative stress
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- lps induced
- lipopolysaccharide induced
- poor prognosis
- cell death
- signaling pathway
- rheumatoid arthritis
- dna damage
- high glucose
- endoplasmic reticulum stress
- immune response
- cell cycle arrest
- drug induced
- skeletal muscle
- liver injury
- binding protein
- cell proliferation
- fluorescent probe
- insulin resistance
- pi k akt
- nitric oxide