Effect of glycosides of cistanche deserticola pretreatment on TLR4 expression in liver tissue of hepatic ischemia-reperfusion injury model rats

Previously, plant extracts of Cistanche deserticola containing glycosides (CGs) were reported to exert antioxidant, anti-apoptotic, hepatoprotective, immunomodulatory, cardiovascular, and neuroprotective effects. Hepatic ischemia-reperfusion (I/R) injury—a pathophysiological occurrence in liver tissue damage—is initiated by the restoration of blood supply to this tissue following interruption of hepatic blood flow. The aim of this study was to investigate the effects of total glycosides derived from C. deserticola on I/R injury in rat liver. Fifty Wistar rats were randomly divided into five groups (n = 10/group): control, hepatic I/R established by surgical occlusion of the left and middle branches of Glisson’s sheath for 60 min and pre-administration of CGs low (25 mg/kg), intermediate (50 mg/kg), or high (100 mg/kg) for 14 d to I/R animals. Serum levels of tumor necrosis factor‑α (TNF‑α) and interleukin‑6 (IL‑6) were measured by ELISA. The protein expressions of TLR4, nuclear factor‑κB P65 (P65), and phosphorylated nuclear factor‑κB P65 (p‑P65) in liver tissues were detected by Western blot. At 60 min after reperfusion, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), TNF‑α, and IL‑6 levels in all CGs‑pretreated groups were significantly lower than (I/R) animals. Hepatic TLR4 protein expression and p‑P65/P65 ratio were significantly decreased in all CGs‑pretreated groups compared to (I/R) animals. CGs may effectively attenuate partial hepatic ischemia‑reperfusion injury in rats by inhibiting activation of the levels of IL-6, TLR4, and NF‑κB, thereby suppressing the inflammatory response. The data suggest that CGs should be considered as a therapeutic agent in the treatment of I/R.