Compared with the RIRI group, the MDA level in the sham group was prominently increased by 78% ( P < 0.01).
Figure 2(a) shows that the level of MDA in the sham group was 56.96 ± 4.62 nmol/kg. Oxidative stress was assessed by measuring MDA, SOD, CAT, GPX, and GSH, which are the end products of lipid peroxidation caused by reactive oxygen species. The purpose of this study was to investigate the protective effect of curcumin in antioxidant stress and inflammation in rats with IRI.
Therefore, curcumin can be used as a new treatment method for renal ischemia-reperfusion (I/R). reported that curcumin markedly inhibited TNF-induced chemokines (CCL2-4, CXCL1, CXCL5, and CXCL8) expression, proinflammatory cytokines (IL-1 α, IL-1 β, and IL-6), and upregulated anti-inflammatory cytokines (IL-4 and IL-13) mRNA expression in visceral adipose tissue, human placenta, and subcutaneous adipose tissue. Curcumin has anti-inflammatory, antioxidant, antifibrosis, anticoagulation, and antitumor activities. Curcumin can reduce renal injury caused by renal ischemia-reperfusion by reducing oxidative stress response, upregulating APPL1 expression, inhibiting the Akt phosphorylation pathway, inhibiting activation of the INOS/NO/CGMP/PKG signaling pathway, inhibiting inflammatory cell infiltration, upregulating HO-1, inhibiting NF- κB activity, and reducing the production of vasoactive substances. It is widely used as food pigment and has good safety in human body. Ĭurcumin is a pigment extracted from turmeric, which is mainly distributed in tropical and subtropical areas such as India, China, and Southeast Asia.
#After effects expressions series#
When renal ischemia-reperfusion occurs, a large number of reactive oxygen species will be produced in the late stage of ischemia-reperfusion, which puts the kidney in a state of high oxidative stress and triggers a series of harmful cellular reactions, leading to inflammatory responses, cell apoptosis, and acute renal failure and even damage to other organs. As an endocrine organ, the kidney is also a hyperperfusion organ, which is particularly sensitive to ischemia and reperfusion. RIRI is a very complex pathological process, which mainly causes kidney damage through mitochondrial damage, inflammation, apoptosis, and oxidative stress. RIRI refers to that after the restoration of blood and oxygen supply to the renal organ after ischemia, the damage of the renal organ is aggravated or even irreversible, usually caused by an inflammatory cascade reaction, including reactive oxygen species (ROS), reactive nitrogen species (RNS), and cytokine, chemokine, and leukocyte activation.
Renal ischemia-reperfusion injury (RIRI) is a common clinical pathological phenomenon, which is commonly seen in vascular surgery and kidney transplantation, and is one of the common causes of acute renal failure. 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. 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. Renal injury was evaluated by measuring the concentration of creatinine (Cr) and urea nitrogen (BUN) in serum. The RIRI group was intraperitoneally administered with normal saline. In the curcumin group, curcumin was intraperitoneally injected once a day for 3 consecutive days using different dosage regimens. 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. Fifty male SD rats (Sprague Dawley) were randomly divided into the sham group, RIRI group, and curcumin group (low, medium, and high).