Patient-related factors related to prolonged preparation-to-colonoscopy interval and insufficient purgative intake before colonoscopy: A post-hoc observational study.

OBJECTIVES: Prolonged preparation-to-colonoscopy (PC) interval and insufficient purgative intake (PI) are two important indicators for quality of bowel preparation for colonoscopy. We aimed to investigate patient-related factors associated with increased PC interval or insufficient PI. METHODS: The post-hoc regression analyses were performed using the data from two prospective studies (NCT04434625 and NCT04101097). Patients receiving reinforced instructions for bowel preparation were recruited. The co-primary outcomes included prolonged PC interval or insufficient PI. RESULTS: Altogether 1806 patients from five endoscopic centers underwent bowel preparation from September 2019 to March 2021. The cut-off values were 6 h for PC interval and 80% for PI. In all, 116 (6.4%) and 73 (4.0%) presented an extended PC interval and insufficient PI, respectively. Multivariate logistic regression analysis showed that a low education level was significantly associated with PC interval ≥6 h. Female sex, body mass index (BMI), and coronary artery disease (CAD) were found to be significantly correlated with insufficient PI in univariate analysis, while multivariate analysis demonstrated BMI <20 kg/m2 (odds ratio [OR] 4.14, 95% confidence interval [CI] 1.92-8.94, P < 0.001) and 20-25 kg/m2 (OR 2.23, 95% CI 1.33-3.73, P = 0.002) and CAD (OR 3.23, 95% CI 1.22-8.53, P = 0.018) were identified as independent risk factors for PI <80%. CONCLUSIONS: In spite of reinforced education, a number of patients did not follow the instructions for bowel preparation. The factors for a prolonged PC interval did not overlap with those for insufficient PI. Individualized interference may be considered in different subpopulations.

Neohesperidin enhances PGC-1α-mediated mitochondrial biogenesis and alleviates hepatic steatosis in high fat diet fed mice.

BACKGROUNDS: Mitochondria plays a critical role in the development and pathogenesis of nonalcoholic fatty liver disease (NAFLD). Neohesperidin (NHP) could lower blood glucose and prevent obesity in mice. However, the direct effect of NHP on hepatic steatosis has not been reported. METHODS: Mice were fed with either a chow diet or HFD with or without oral gavage of NHP for 12 weeks. A variety of biochemical and histological indicators were examined. In vitro cell culture model was utilized to demonstrate underlying molecular mechanism of the effect induced by NHP treatment. RESULTS: NHP increases mitochondrial biogenesis, improves hepatic steatosis and systematic insulin resistance in high fat diet (HFD) fed mice. NHP elevates hepatic mitochondrial biogenesis and fatty acid oxidation by increasing PGC-1α expression. Mechanistically, the activation of AMP-activated protein kinase (AMPK) is involved in NHP induced PGC-1α expression. CONCLUSIONS: PGC-1α-mediated mitochondrial biogenesis plays a vital role in the mitigation of hepatic steatosis treated by NHP. Our result suggests that NHP is a good candidate to be dietary supplement for the auxiliary treatment of NAFLD.

Astilbin ameliorates cisplatin-induced nephrotoxicity through reducing oxidative stress and inflammation.

Oxidative stress and inflammation are considered to be the main pathogenesis of cisplatin nephrotoxicity. Astilbin, a flavonoid with anti-oxidation and anti-inflammation function, has been used to treat heavy metal induced kidney injury. In this study, we investigated the protective effects of astilbin on cisplatin-induced nephrotoxicity and its underlying mechanisms. Our results showed that astilbin markedly inhibited cisplatin-induced cell apoptosis and recovered cell growth. Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293 cell apoptosis. Astilbin effectively enhanced NRF2 activation and transcription of its targeting antioxidant genes to reduce ROS accumulation in cisplatin-induced HEK-293 cells. Furthermore, we found that astilbin obviously suppressed tumor necrosis factor alpha (TNF-α) expression and NF-κB activation, and also inhibited the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Finally, we confirmed that the effect of astilbin to improve renal oxidative stress and inflammation in cisplatin induced acute nephrotoxic mice. In conclusion, our study suggests that astilbin could ameliorate the cisplatin-induced nephrotoxicity by reducing oxidative stress and inflammation.