Notoginsenoside R1 Attenuates Renal Ischemia-Reperfusion Injury in Rats

Abstract

Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury. As an effective element of Panax notoginseng, NR1 has antioxidant, anti-inflammatory, antiapoptotic, and immune-stimulatory activities. Therefore, we speculate that NR1 can attenuate renal I/R injury. Ischemia-reperfusion injury was induced by renal pedicle ligation followed by reperfusion along with a contralateral nephrectomy. Male Sprague-Dawley rats were randomized to four groups: sham group, I/R control group, NR1-1 group (rats treated with NR1, 20 mg.kg.d) and NR1-2 group (rats treated with NR1, 40 mg.kg.d). All animals were killed 72 h after I/R induction. Blood and renal tissues were collected. Renal dysfunction was observed by the level of serum creatinine and histological evaluation. Apoptosis and inflammatory response in the tissue of kidney were detected mainly with molecular biological methods. NR1 attenuated I/R-induced renal dysfunction as indicated by the level of serum creatinine and histological evaluation. It prevented the I/R-induced increases in the levels of proinflammatory cytokine TNF-alpha, myeloperoxidase activity, phosphorylation of p38, and activation of nuclear factor kappaB with cell apoptosis in the kidney and enhanced expression of antiapoptosis cytokine bcl-2. Treatment with NR1 improves renal function after I/R associated with a significant reduction in cell apoptosis and inflammatory responses, which may be related to p38 and nuclear factor kappaB inhibition.

Up-Regulation of HMGB1 Exacerbates Renal Ischemia-Reperfusion Injury by Stimulating Inflammatory and Immune Responses through the TLR4 Signaling Pathway in Mice

“…Rodriguez-Peña et al who explained that the initial pathological events in renal I/R include vasoconstriction, endothelial cell activation, tubular desquamation and swelling, necrosis of the tubular epithelium, and interstitial edema [17], giving way to the progression of the inflammatory process, a major cause of I/R-induced tissue injury [18,19]. The necrotic cells triggered by the lack of oxygen and nutrients in ischemic process can greatly stimulate immune responses and result in the infiltration of inflammatory cells and the production of cytokines [20].…”

Notoginsenoside R1 Protects against Neonatal Cerebral Hypoxic-Ischemic Injury through Estrogen Receptor-Dependent Activation of Endoplasmic Reticulum Stress Pathways

“…Panax notoginseng is believed to have anti-inflammatory, antioxidative, and antiapoptotic properties (Liu et al, 2010. In the study by Zhang et al (2015) study, NGR1 could attenuate inflammatory bowel disease via the pregnane X receptor.…”

Renoprotective effect of aliskiren on renal ischemia/reperfusion injury in rats: electron microscopy and molecular study

“…53 The I/R also increases the release of NF-kb in the kidney tissue. 54,55 In one study, it was shown that captopril application inhibited the NF-kb signal pathway and decreased the TNF-a and iNOS. 56,57 Therefore, ACE inhibitors and AT-2 antagonist inhibition can be used in preventing chronic complications induced by disease.…”