scholarly journals Curcumin Protects against Renal Ischemia/Reperfusion Injury by Regulating Oxidative Stress and Inflammatory Response

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xiaoying Cui ◽  
Lili Lin ◽  
Xiaoling Sun ◽  
Lin Wang ◽  
Rong Shen
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Renal Injury ◽  
Iron Reduction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Inflammatory Factors ◽  
Left Renal Artery ◽  
Contralateral Kidney

Objective. The aim of this study was to explore the pharmacological effects of curcumin on oxidative stress and inflammatory response of renal dysfunction induced by renal ischemia/reperfusion (RIRI). Methods. Fifty male SD rats (Sprague Dawley) were randomly divided into the sham group, RIRI group, and curcumin group (low, medium, and high). The RIRI model was established by clipping the left renal artery for 45 min and then reperfusion for 24 h and resection of the contralateral kidney. In the curcumin group, curcumin was intraperitoneally injected once a day for 3 consecutive days using different dosage regimens. The RIRI group was intraperitoneally administered with normal saline. Renal injury was evaluated by measuring the concentration of creatinine (Cr) and urea nitrogen (BUN) in serum. Oxidative stress was assessed by assessing the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), and iron reduction/antioxidant capacity (FRAP) in tissues. In addition, the protective effect of RIRI was investigated by measuring Paller scores, the level of serum inflammatory factors and caspase-3, and the number of apoptotic cells. Results. Ischemia/reperfusion resulted in increased levels of Cr and BUN in serum and MDA in tissues and decreased levels of SOD, CAT, GPx, GSH, and FRAP. Curcumin pretreatment strikingly increased the level of SOD, CAT, GPx, GSH, IL-10, IFN-γ, and FRAP and significantly decreased MDA, Cr, BUN, IL-8, TNF-α, IL-6, and myeloperoxidase (MPO) expressions in tissues. Conclusion. Curcumin can relieve the degree of renal injury and improve renal function in ischemia-reperfusion, which may be related to the fact that curcumin can increase SOD content in serum and reduce MDA and FRAP levels in the rat model.

scholarly journals The Protective Effect of Anthocyanins Extracted from Aronia Melanocarpa Berry in Renal Ischemia-Reperfusion Injury in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Li Li ◽  
Jun Li ◽  
Hui Xu ◽  
Fengmei Zhu ◽  
Zhijun Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Reperfusion Injury ◽  
Renal Dysfunction ◽  
Proinflammatory Cytokines ◽  
Renal Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Aronia Melanocarpa

Background. Our previous research showed the antioxidant activity of anthocyanins extracted from Aronia melanocarpa of black chokeberry in vitro. Ischemia acute kidney injury is a significant risk in developing progressive and deterioration of renal function leading to clinic chronic kidney disease. There were many attempts to protect the kidney against this progression of renal damage. Current study was designed to examine the effect of pretreatment with three anthocyanins named cyanidin-3-arabinoside, cyanidin-3-glucodise, and cyaniding-3-galactoside against acute ischemia-reperfusion injury in mouse kidney. Methods. Acute renal injury model was initiated by 30 min clamping bilateral renal pedicle and followed by 24-hour reperfusion in C57Bl/6J mice. Four groups of mice were orally pretreated in 50 mg/g/12 h for two weeks with cyanidin-3-arabinoside, cyanidin-3-glucodise, and cyaniding-3-galactoside and anthocyanins (three-cyanidin mixture), respectively, sham-control group and the renal injury-untreated groups only with saline. Results. The model resulted in renal dysfunction with high serum creatinine, blood urea nitrogen, and changes in proinflammatory cytokines (TNF-ɑ, IL-1β, IL-6, and MCP-1), renal oxidative stress (SOD, GSH, and CAT), lipid peroxidation (TBARS and MDA), and apoptosis (caspase-9). Pretreatment of two weeks resulted in different extent amelioration of renal dysfunction and tubular damage and suppression of proinflammatory cytokines, oxidative stress, lipid peroxidation, and apoptosis, thus suggesting that cyanidins are potentially effective in acute renal ischemia by the decrease of inflammation, oxidative stress, and lipid peroxidation, as well as apoptosis. Conclusion. the current study provided the first attempt to investigate the role of anthocyanins purified from Aronia melanocarpa berry in amelioration of acute renal failure via antioxidant and cytoprotective effects.

Etomidate Alleviates Ischemia-Anoxia Reperfusion Injury in Intestinal Epithelial Cells by Inhibiting the Activation of traf6-Regulated NF-KB Signaling

2022 ◽  
Vol 12 (5) ◽  
pp. 1015-1021
Author(s):  
Gen Lin ◽  
Ruichun Long ◽  
Xiaoqing Yang ◽  
Songsong Mao ◽  
Hongying Li
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Intestinal Epithelial Cells ◽  
Ischemia Reperfusion ◽  
Stress Factors ◽  
Inflammatory Factors ◽  
Intestinal Cell ◽  
Intestinal Epithelial

Objective: The present study aimed to investigate the role of etomidate in intestinal cell ischemia and hypoxia-reperfusion injury and potential mechanisms. Method: In this study, we establish the intestinal epithelial cells ischemia-reperfusion model in vitro. CCK8 was used to detect cell viability and flow cytometry assay was used to detect apoptosis levels of treated OGD/R model cells. ELISA measured the expression level of oxidative stress factors and inflammatory factors. Furthermore, western blot assay was used to detect the expression the apoptosis-related factors and TNFR-associated factors in treated OGD/R model cells. Result: Etomidate does not affect the activity of intestinal epithelial cells, and can protect intestinal epithelial cells to reduce ischemiareperfusion injury, and the expression of inflammatory factors and oxidative stress in cells with mild intestinal epithelial ischemia-reperfusion injury. Etomidate alleviates apoptosis of intestinal epithelial ischemia-reperfusion injury cells. Etomidate inhibits the activation of traf6-mediated NF-κB signal during ischemia-anoxia reperfusion of intestinal epithelial cells. Conclusion: Taken together, our study demonstrated that etomidate attenuates inflammatory response and apoptosis in intestinal epithelial cells during ischemic hypoxia-reperfusion injury and inhibits activation of NF-κB signaling regulated by TRAF6.

Hydrogen Sulfide Reduces Renal Ischemia-Reperfusion Injury by Enhancing Autophagy and Reducing Oxidative Stress

2021 ◽  
Author(s):  
Hui Li ◽  
Shuaiwei Wang ◽  
Shuangshuang An ◽  
Biao Gao ◽  
Tieshan Teng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Beclin 1 ◽  
Dependent Manner ◽  
Protein Levels ◽  
Renal Ischemia Reperfusion Injury

Abstract Background Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury. Hydrogen sulfide (H2S) exerts a protective effect in renal IRI. The present study was carried out to investigate the effects of exogenous H2S on renal IRI by regulating autophagy in mice. Methods Mice were randomly assigned to control, IRI, and NaHS (28, 56 and 100 µmol/kg) groups. Renal IRI was induced by clamping the bilateral renal pedicles for with non-traumatic arterial clamp for 45 min and then reperfused for 24 h. Mice were administered intraperitoneally with NaHS 20 min prior to renal ischemia. Sham group mice underwent the same procedures without clamping. Serum and kidney tissues were harvested 24 h after reperfusion for functional, histological, oxidative stress, and autophagic determination. Results Compared with the control group, the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN), and malondialdehyde (MDA), the protein levels of LC3II/I, Beclin-1, and P62, as well as the number of autophagosomes were significantly increased, but the activity of superoxide dismutase (SOD) was decreased after renal IRI. NaHS pretreatment dramatically attenuated renal IRI-induced renal dysfunction, histological changes, MDA concentration, and p62 expression in a dose-dependent manner. However, NaHS increased the SOD activity and the protein levels of LC3II/I and Beclin-1. Conclusions These results indicate that exogenous H2S protects the kidney from IRI through enhancement of autophagy and reduction of oxidative stress. Novel H2S donors could be developed in the treatment of renal IRI.

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