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Ginsenoside Rb1 attenuates intestinal ischemia reperfusion induced renal injury by activating Nrf2/ARE pathway
Qian Sun1, Qing-Tao Meng, Ying Jiang
1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Abstract:
Intestinal ischemia reperfusion (IIR) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The aim of this study was to investigate the effects of ginsenoside Rb1 on IIR induced renal injury in mice. An intestinal ischemia reperfusion mouse model was established by superior mesenteric artery (SMA) occlusion for 45 min, followed by reperfusion for 2 h. IIR induced renal injury characterized by increase of BUN, Cr and NGAL in serum, MDA levels and decrease of SOD levels in the renal tissues. Ginsenoside Rb1 (30, 60 mg/kg) given intraperitoneally before reperfusion attennuated renal injury, which was associated with decrease of BUN, Cr and NGAL in serum, MDA levels and increase of SOD levels in the renal tissues. Furthermore, the immunohistochemistry and Western blot data showed that ginsenoside Rb1 dramatically reversed IIR induced renal injury, associated with upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in renal tissues. Our data suggests that ginsenoside Rb1 attenuates acute renal injury induced by intestinal ischemia reperfusion by activating the Nrf2/ARE pathway.
Insights
Ginsenoside Rb1 protects against kidney damage from intestinal ischemia reperfusion (IIR) in mice. This compound activates the Nrf2/ARE pathway, reducing oxidative stress and improving renal function after IIR injury.
Area of Science:
- Nephrology
- Gastroenterology
- Pharmacology
Background:
- Intestinal ischemia reperfusion (IIR) is a critical condition leading to multi-organ dysfunction.
- Renal injury is a common and severe complication of IIR.
- Investigating protective agents for IIR-induced renal damage is clinically significant.
Purpose of the Study:
- To evaluate the protective effects of ginsenoside Rb1 against acute kidney injury induced by IIR in a mouse model.
- To elucidate the underlying molecular mechanisms of ginsenoside Rb1's renoprotective action.
Main Methods:
- Establishment of an IIR mouse model via superior mesenteric artery occlusion and reperfusion.
- Administration of ginsenoside Rb1 (30, 60 mg/kg) prior to reperfusion.
- Assessment of renal injury markers (BUN, Cr, NGAL, MDA, SOD) and molecular pathways (Nrf2, HO-1) using biochemical assays, immunohistochemistry, and Western blot.
Main Results:
- IIR significantly increased serum BUN, Cr, NGAL, and renal MDA levels, while decreasing SOD levels.
- Ginsenoside Rb1 treatment dose-dependently attenuated these IIR-induced changes.
- Ginsenoside Rb1 upregulated the expression of Nrf2 and HO-1 in renal tissues.
Conclusions:
- Ginsenoside Rb1 demonstrates significant renoprotective effects against IIR-induced acute kidney injury in mice.
- The protective mechanism involves the activation of the Nrf2/ARE pathway, leading to reduced oxidative stress.
- Ginsenoside Rb1 holds potential as a therapeutic agent for managing IIR-related renal complications.
