Ethanol (EtOH) is a common trigger for gastric mucosal diseases, and mitigating oxidative stress is essential for attenuating gastric mucosal damage. Capsaicin (CAP) has been identified as a potential agent to counteract oxidative damage in the gastric mucosa; however, its precise mechanism remains unclear. This study demonstrates that CAP alleviates EtOH-induced gastric mucosal injuries through two primary pathways: by suppressing the chemokine receptor 4 (CCR4)/Src/p47phox axis, thereby reducing oxidative stress, and by inhibiting the phosphorylation and nuclear translocation of nuclear factor-κB p65 (NF-κB) p65, resulting in diminished inflammatory responses. These findings elucidate the mechanistic pathways of CAP and provide a theoretical foundation for its potential therapeutic application in the treatment of gastric mucosal injuries.
Ethanol/toxicity* ; Animals ; Gastric Mucosa/metabolism* ; Signal Transduction/drug effects* ; Oxidative Stress/drug effects* ; Capsaicin/pharmacology* ; Male ; NADPH Oxidases/genetics* ; Mice ; Humans ; src-Family Kinases/genetics*

AIM To investigate the improving effects of epigallocatechin gallate (EGCG) on rat kidney injury induced by cisplatin and its mechanism of action.METHODS Fifty male SD rats (10 rats/group) were randomly divided into blank control group,kidney injury group,EGCG low-,middle-and high-dose (25,50 and 100 mg/kg) groups.The kidney injury group and the drug administration group were treated with 7.5 mg/kg cisplatin by intraperitoneal injection to build the kidney injury model,and the blank control group was intraperitoneally injected with normal saline.After fourteen days of administration,the general condition and morphological changes of kidney tissue by HE staining were observed;BUN,Cr,Cys-c contents in serum,and IL-18,KIM-1 contents in urine were detected by ELISA;MDA,GSH and T-SOD contents in renal cortex were determined by kit;Western blot method was used to determine the contents of Nrf2 protein in renal contex cytoplasm and nucleus,and the expression level of HO-1 protein.RESULTS EGCG intervention could improve the pathological structural changes of rat kidney injury induced by cisplatin,decrease kidney index,and decrease serum Cr,Cys-c contents and urine IL-18,KIM-1 contents.Moreover,renal cortex MDA concentration decreased,and renal cortex GSH concentration,T-SOD activity increased.At the same time,renal cortex cytoplasm Nrf2 content reduced,but nucleus Nrf2 and total cell HO-1 contents increased.CONCLUSION EGCG plays a role in the improvement of rat kidney injury induced by cisplatin through the activation of Nrf2/HO-1 signal pathway.