Abstract
Ganoderma lucidum polysaccharide peptide (GLPP) scavenges oxygen free radicals that are a key factor in the pathogenesis of renal ischemia reperfusion injury (RIRI). The aim of this study was to determine whether GLPP could attenuate RIRI by counteracting the oxidative stress. The mechanism involved was assessed by an in vivo mouse RIRI model and an in vitro hypoxia/reoxygenation model, and tunicamycin-stimulated NRK-52E cells were used to explore the GLPP-mediated alleviation of ER stress. Experimental results showed that renal dysfunction and morphological damage were reduced in GLPP-treated group. The imbalance of redox status was reversed and production of ROS was reduced by GLPP. RIRI-induced mitochondrial- and ER stress-dependent apoptosis were dramatically inhibited in GLPP-treated group. Intriguingly, JNK activation in the kidney with RIRI or hypoxia/reoxygenation was inhibited by GLPP. These results suggest that the protective effect of GLPP against RIRI may be due to reducing oxidative stress, alleviating the mitochondrial and ER stress-dependent apoptosis caused by excessive ROS.
Highlights
The aim of this study was to determine whether Ganoderma lucidum polysaccharide peptide (GLPP) could protect kidneys against renal ischemia reperfusion injury (RIRI) and to elucidate the related mechanisms
GLPP restored the balance of oxidative stress induced by ischemia reperfusion (IR), indicating a protective effect of GLPP against IR, likely related to improvement in the endogenous antioxidant system
We found that the increased ROS production and decreased Mn-superoxide dismutase (SOD) expression caused by IR or H/R were reversed by GLPP
Summary
Clinical and experimental studies have discovered that ROS play a vital role in tissue damage and cell apoptosis during IR, during the process of reperfusion. During the process of RIRI, the mitochondria are the major sources and targets of ROS. Oxidative stress interferes with redox-dependent reactions and with protein folding, resulting in protein misfolding in the endoplasmic reticulum (ER)[17]. Altered redox homeostasis in the ER is sufficient to cause ER stress, which in turn induces the production of ROS, both in the ER and in the mitochondria. Several studies have proven that ER stress and mitochondrial dysfunction are intimately linked to the pathogenesis of RIRI18. We proposed that GLPP may prevent and alleviate RIRI by restoring the balance of the oxidation/antioxidant system. The experimental results showed that GLPP could prevent RIRI, indicating that GLPP may be developed as a candidate drug for preventing RIRI
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