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00, 95% CI = 0.76-1.30, p = 0.284). Positive PD-L1 expression was significantly correlated with sex (RR = 1.22, 95% CI = 1.07-1.38, p = 0.002), histological differentiation (RR = 1.15, 95% CI = 1.02-1.30, p = 0.020), distant metastasis (RR = 0.68, 95% CI = 0.54-0.86, p = 0.011), lymph node metastasis status (RR = 0.83, 95% CI = 0.76-0.91, p less then 0.001), TNM stage (RR = 0.81, 95% CI = 0.73-0.89, p less then 0.001), and human papilloma virus infection status (RR = 1.30, 95% CI = 1.04-1.62, p = 0.019), but was not correlated with T stage and tumor recurrence. Glycyrrhizin ic50 CONCLUSION High PD-L1 expression in OSCC was not related to OS. However, high PD-L1 expression was significantly related to certain clinicopathological features. Thus, positive PD-L1 expression may be a biomarker of poor prognosis in patients with OSCC. OBJECTIVE The study was aimed to explore the hepatocellular protective functions of cafestol during hepatic ischemia-reperfusion injury and the possible mechanisms. METHODS Ninety male Balb/c mice were randomly divided into seven groups, including normal control group, L-cafestol(20mg/kg) group, H-cafestol(40mg/kg) group, sham group, IR group, L-cafestol(20mg/kg) + IR group, H-cafestol(40mg/kg) + IR group. Serum liver enzymes (ALT, AST), inflammation mediators, proteins associated with apoptosis and autophagy, indicators linked with ERK/PPARγ pathway, and liver histopathology were measured using ELISA, qRT-PCR, immunohistochemical staining, and western blotting at 2, 8, and 24 hours after reperfusion. RESULTS Our findings confirmed that cafestol preconditioning groups could reduce the levels of ALT and AST, alleviate liver pathological damage, suppress the release of inflammation mediators, inhibit the production of pro-apoptosis protein including caspase-3, caspase-9 and Bax, decrease the expression of autophagy-linked protein including Beclin-1 and LC3, increase anti-apoptosis protein Bcl-2, and restrain the activation of ERK and PPARγ. CONCLUSION Cafestol preconditioning could attenuate inflammatory response, apoptosis and autophagy on hepatic ischemia reperfusion injury by suppressing ERK/PPARγ pathway. Diabetic nephropathy (DN), a common microvascular complication of type 2 diabetes mellitus (T2DM), causes increasing mortality and morbidity due to its high prevalence and severe consequences. Hence, it is urgent to search for effective agents that provide new insights into novel molecular therapeutic targets for DN. This study was designed to investigate the critical role of Akebia saponin D (ASD) in kidney damage, inflammation and apoptosis of renal tubular cells in DN. To probe the protective effects of ASD on DN in vivo, diabetes mellitus model was established by intraperitoneal (ip) injection of STZ (60 mg/kg) for 5 days consecutively. Besides, HG-induced human renal tubular cells (HK-2) were used to analyze the defined effects and underlying mechanism of ASD on DN in vitro. Blood glucose, insulin, serum creatinine (Scr), blood urea nitrogen (BUN), renal injury, inflammation, oxidative stress and apoptosis of renal tubular cells were respectively measured and evaluated. ASD prevented kidney damage, improved renal function and inflammatory reaction, ameliorated oxidative stress and inhibited apoptosis of renal tubular cells in DN mice via activation of NRF2/HO-1 pathway and inhibition of NF-KB pathway. IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Previous studies reveal that genetic factors play a crucial role in IgAN progression. This study was conducted to investigate the association between MIR31HG variants and IgAN risk. A total of 836 subjects were recruited to detect the relationship of MIR31HG variants with IgAN susceptibility. Odds ratios (OR) and 95% confidence intervals (CI) were computed to evaluate the associations. Multifactor dimensionality reduction was performed to analyze the SNP-SNP interaction with IgAN risk. Our study showed that rs1332184 and rs55683539 significantly related to an increased risk of IgAN (OR 1.34, p = 0.041; OR 1.39, p = 0.025). Stratified analyses indicated rs72703442, rs55683539, and rs10965064 exhibited strongly enhanced risk of IgAN in age ≤ 35 years (OR 1.55, p = 0.023; OR 1.60, p = 0.012; OR 1.46, p = 0.037). Besides, we found rs1332184, rs55683539 and rs2181559 significantly increased the susceptibility of IgAN in males (OR 1.71, p = 0.003; OR 1.44, p = 0.042; OR 1.60, p = 0.010). We also observed that rs1332184 could enhance IgAN risk for Lee's grade ≥ III (OR 1.39, p = 0.045). Rs55683539 significantly increased a risk of IgAN (OR 1.58, p = 0.027), while rs2025327 had a lower risk of IgAN in Lee's grade less then III (OR 0.46, p = 0.007). Interestingly, we found rs72703442 polymorphism was related to hemoglobin (p = 0.043), and rs10965064 was associated with Urine red blood cell (p = 0.040). Our study proposed that MIR31HG polymorphisms associate with susceptibility to IgAN in Chinese population. The effects of Na2CO3 on the quality, change of protein subunits and volatile compounds of sourdough leavened Chinese steamed bread (sourdough-CSB) and yeast leavened CSB (yeast-CSB) were investigated. Results suggested that, low Na2CO3 level endowed both CSB with softer crumb and little change of surface color. Besides, Na2CO3 addition improved the overall aroma profile by inhibiting the production of aroma-negative compounds (butanoic acid, 1-octen-3-ol, hexanal and heptanal). Sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis showed an obvious increase in intensity of protein bands with low molecular weight, consistent with the result of size-exclusion high-performance liquid chromatography analysis and free sulfhydryl group (SH) content, indicating the hydrolysis of glutenin macropolymer (GMP) under alkaline condition in yeast-CSB. While in sourdough-CSB, GMP and SH content firstly decreased at low Na2CO3 level (0-0.2%) and then increased at high Na2CO3 level (0.3%-0.5%). This study aimed to investigate if myo-inositol (MI) supplementation could alleviate adverse effects caused by aflatoxin B1 (AFB1) with respect to growth performance, AFB1 residues, immune response and antioxidant status of Litopenaeus vannamei. 800 shrimp (initial weight 1.1 g) were divided into five groups MI0 (basal diet); MI0 + LA, MI0 + HA, MI200 + LA and MI200 + HA fed with AFB1-contaminated diets (LA, low concentration AFB1; HA, high concentration AFB1; MI200, adding 200 mg MI kg-1 diet). The results showed that HA significantly decreased growth performance, systemic inositol content and lipid content. AFB1 residues were detected in the hepatopancreas of shrimp, but not the muscle. Histological lesions were observed in MI0 + LA and MI0 + HA groups. HA supplementation raised malondialdehyde and protein carbonyl content and reduced some antioxidant enzyme activities and immune-related genes expression, which was slightly ameliorated by MI supplementation. Our results suggest that myo-inositol may slightly mitigate negative impacts caused by AFB1 in L.
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