Ischaemia-reperfusion injury (IRI) is the predominant cause of acute kidney injury. Nevertheless, the underlying molecular mechanisms are still unclear. The current study investigated the effects of nicorandil on ATP-sensitive potassium (K_ATP) channels and the potential signal transduction pathway(s) in a rat kidney IRI model and in cultured tubular HK-2 cells subjected to oxygen and glucose deprivation/reoxygenation (OGD/R) injury. The standard procedure for IRI was performed in newborn rat kidneys. Pretreatment with nicorandil (10 mg/kg) 2 h prior to induction of IRI improved renal function, attenuated tubule damage, and prevented apoptosis of tubule cells, infiltration of neutrophils and macrophages, and production of inflammatory cytokines interleukin (IL)-6, IL-17 and tumour necrosis factor-a. Ischaemia-reperfusion-induced reduction of K_IR6.2 was restored to normal levels by nicorandil. The activation of the phosphoinositide-3-kinase (PI3K)-Akt-nuclear factor (NF)-κB axis was detected in this rat kidney IRI model, which was blocked by nicorandil. The renoprotection of nicorandil against IRI was abolished by its inhibitor glibenclamide (1 mg/kg). Similar results were obtained in OGD/R-damaged HK-2 cells. Taken together, our findings demonstrated the specific renoprotective role of nicorandil in the newborn rat IRI kidney by decreasing the production of inflammatory cytokines, and restoring the expression of K_IR6.2 potentially through the PI3K-Akt-NF-κB axis.

Objectives. To investigate whether Helicobacter pylori (H. pylori) infection increases the risk of colorectal adenomatous polyp (CAP) in the context of age and gender. Methods. A total of 563 study subjects (male/female, 368/195) from Beijing, China, with higher nursing level who underwent colonoscopy were retrospectively collected. H. pylori and CAP were detected by carbon-13 urea breath test and colorectal colonoscopy. The correlations between the number, size, distribution, and pathological grade of CAP and H. pylori infection were analyzed. The population was further stratified by age and gender in order to examine the risk of H. pylori and CAP in the context of these variables. The influence of H. pylori on the risk of CAP was assessed by logistic regression model. Results. 315 participants were diagnosed with CAP, and 207 participants were classified as healthy controls. The prevalence of H. pylori in the CAP group was significantly higher than that in the healthy control group (119/315, 37.8% versus 44/207, 21.3%) (p<0.001). The proportion of H. pylori positive plus CAP in participants <50 years old was significantly higher than that in participants >50 years old (87/250; 34.8% versus 32/65; 49.2%) (p=0.033). Furthermore, H. pylori infection was identified as one of the major risk factors of CAP (OR=2.679; 95% CI: 1.717-4.179, p<0.001), independent of age, sex, and body mass index and was correlated with size, distribution, and pathological grading of CAP (p<0.001). Conclusions. H. pylori is a major risk factor for CAP. Further studies are needed to assess the effects of H. pylori treatment or persistent infection on the occurrence or recurrence of CAP.

Background. Previous studies have suggested a link between Helicobacter pylori (H. pylori) infection and nonalcoholic fatty liver disease (NAFLD), yet long-term follow-up studies to elucidate this association are lacking. We aimed to identify the relationship between NAFLD and H. pylori in these people. Methods. A total of 2,934 adults between June 2013 and October 2017 were collected; among them, 675 people met the requirements. People were assessed for H. pylori infection diagnosis as detected by the carbon-13 urea breath test; they were also assessed for NAFLD diagnosis by ultrasound. Results. H. pylori infection was present in 206 patients (30.5%), and 469 (69.5%) participants were classified as controls. Participants with H. pylori infection had a higher rate of incident NAFLD than those who were uninfected (37/206; 18% versus 73/469; 15.6%) ( p < 0.001 ). Compared with the control group, the recovery rate of NAFLD in the H. pylori+ve group was low (6/206, 2.9% versus 33/469, 7.0%) ( p < 0.001 ). Besides, the incidence of uric acid, postprandial blood glucose, TG, LDL-C, HDL-C, and fasting plasma glucose was significantly different between the two groups ( p < 0.001 ), but no difference was found in alanine aminotransferase (ALT), liver-total protein, urea nitrogen, and cholesterol ( p > 0.05 ). Conclusion. H. pylori infection was a risk factor for NAFLD and affected the occurrence or reversal of NAFLD, indicating that H. pylori infection eradication might play a role in reducing the risk of NAFLD.