Abstract
Ginsenoside Rb1 (GRb1), one of the major active saponins isolated from ginseng, has recently been reported to protect various organs against ischemia/reperfusion (IR) injury; however, the mechanisms underlying these protective effects following intestinal IR (IIR) remain unclear. The present study aimed to evaluate the effects of GRb1 on IIR injury and determine the mechanisms involved in these effects. Sprague Dawley rats were subjected to 75 min of superior mesenteric artery occlusion, followed by 3 h of reperfusion. GRb1 (15 mg/kg) was administered intraperitoneally 1 h prior to the induction of IIR, with or without intravenous administration of Wortmannin [WM; a phosphoinositide 3‑kinase (PI3K) inhibitor, 0.6 mg/kg]. The degree of intestinal injury and oxidative stress‑induced damage was determined by histopathologic evaluation and measurement of the serum activity levels of D‑lactate, diamine oxidase and endotoxin, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and 8‑iso‑prostaglandin F2α (8‑iso‑PGF2α). The protein expression levels of p85, phosphorylated (p)‑p85, protein kinase B (Akt), p‑Akt and nuclear factor erythroid 2‑related factor 2 (Nrf2) were determined via western blotting, and the concentrations of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β and IL‑6 were measured via ELISA. It was revealed that IIR led to severe intestinal injury (as determined by significant increases in intestinal Chiu scores), which was accompanied with disruptions in the integrity of the intestinal mucosal barrier. IIR also increased the expression levels of TNF‑α, IL‑1β, IL‑6, MDA and 8‑iso‑PGF2α in the intestine, and decreased those of SOD. GRb1 reduced intestinal histological injury, and suppressed inflammatory responses and oxidative stress. Additionally, the protective effects of GRb1 were eliminated by WM. These findings indicated that GRb1 may ameliorate IIR injury by activating the PI3K/protein kinase B/Nrf2 pathway.