Background/Aims: Diabetic nephropathy is a common complication of diabetes. This study explored the renal protective effect and possible mechanism of gliquidone in mice with diabetic nephropathy. Methods: Animal model of diabetic nephropathy was established in KKAy mice. The renal protective effect of gliquidone was studied by evaluating the kidney function through measures of urinary protein, blood urea nitrogen (BUN), serum creatinine (Scr) and serum triglyceride (TG) that were performed using an automatic biochemical analyzer. The levels of oxidative stress indicators, such as nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA), were evaluated in renal tissue homogenates using the automatic biochemical analyzer. The inhibitory effect of gliquidone on renal interstitial fibrosis and its association with Notch / Snail1 signaling pathway in diabetic nephropathy was investigated using molecular biological techniques. Results: It was found that low-, medium- and high-dose gliquidone improved the mice’s general health condition, such as mental status, fur condition, eating, and drinking. Gliquidone reduced the body weight and the kidney weight /body weight ratio of mice. Gliquidone improved the kidney function, indicated by reductions in urinary protein, blood urea nitrogen, and serum creatinine and triglyceride. Gliquidone treatment increased levels of nitric oxide and superoxide dismutase, but decreased level of malondialdehyde. The expression of Jagged1/Notch1/hes1/Snail1/α-SMA decreased, while the expression of E-cadherin increased in gliquidone-treated kidneys. High dose gliquidone showed the best effect, one that was similar to that of the positive control drug irbesartan. Conclusion: Taken together, our results suggested that gliquidone can ameliorate the diabetic symptoms of diabetic nephropathy through inhibiting Notch / Snail1 signaling pathway, improving anti -oxidative response and delaying renal interstitial fibrosis. The efficacy of gliquidone is dose-dependent.
Objectives: This study further compared the endoscopic retrograde cholangiopancreatography (ERCP) and laparoscopic transcystic common bile duct exploration (LTCBDE) approaches in the treatment of common bile duct stones (CBDS) from the perspective of efficacy, safety and economy.Methods: The therapeutic efficacy and safety of ERCP and LTCBDE approaches were retrospectively compared. Cost-effectiveness analysis of clinical economics was performed to analyze and evaluate the two approaches.Results: There was no significant difference in the success rate of surgery and bile stone residue between ERCP and LTCBDE group. The incidence of postoperative complications in ERCP group was significantly higher than that in the LTCBDE group; while the incidence of pancreatitis in the ERCP group was significantly higher than that in the LTCBDE group. There was no significant difference in biliary infection, bile leakage and sepsis between ERCP and LTCBDE groups. In terms of cost, the costs of surgery and nursing were significantly lower, the costs of treatment and sanitary materials were significantly higher in the ERCP group than that in the LTCBDE group. There was no significant difference in the costs of medical examination, laboratory test, medicine cost and total cost between ERCP group and LTCBDE group. The total length of hospital stay, length of hospital stay before surgery and duration of surgery in the ERCP group were significantly lower than that in the LTCBDE group; there was no significant difference in length of hospital stay after surgery between the ERCP and LTCBDE group. The cost-effectiveness ratio of ERCP group was 34171.25, and the cost-effectiveness of LTCBDE group was 34524.25. The incremental cost-effectiveness ratio (ICER) of the two groups was 51415.Conclusion: ERCP and LTCBDE approaches had similar therapeutic efficacy in the treatment of CBDS. The safety of LTCBDE approach is superior to that of ERCP approach for the treatment of CBDS. ERCP approach is more economical in the treatment of CBDS than LTCBDE approach.
This work carried out comprehensive bioinformatics analysis and explored potential actions of COL22A1 in hepatocellular carcinoma (HCC) pathophysiology. Methods: Microarray datasets including GSE159220, GSE104766, GSE104310 and GSE33294 were retrieved for bioinformatics analysis. Overlapped differentially expressed genes (DEGs) among GSE159220, GSE104766, GSE104310 and GSE33294 were first subjected to functional annotation analysis. Protein-protein interaction (PPI) network was constructed to reveal the hub genes in the network. The miRNAs-mRNA from hub genes were also constructed. Prognostic analysis of patients with HCC was undertaken to evaluate prognostic values of these hub genes. Functional assays were employed to determine actions of COL22A1 in the HCC cell progression.Results: Ninety-one common up-regulated DEGs and 55 common down-regulated DEGs among GSE159220, GSE104766, GSE104310 and GSE33294 were identified. Functional annotation analysis revealed that these common DEGs may be correlated with the extracellular matrix. The protein-protein interaction analysis further revealed 20 hub genes. Among these hub genes, high expression levels of COL2A1, COL22A1, HAPLN1, PTHLH and SOX2 showed positive associatin with shorter overall survival (OS) of HCC patients, while low expression levels of COL17A1, REN and TRH exhibited correlation with shorter OS of HCC patients. Furthermore, the COL22A1 was overexpressed in HCC tissues when compared to normal ones, and the promoter methylation level of COL22A1 was significantly lower in the HCC tissues when compared to normal ones. Validation assays deciphered that COL22A1 silencing suppressed HCC cell invasion, migration and epithelial mesenchymal transition. Conclusion: This study identified several hub genes closely correlated with HCC pathogenesis, and COL22A1 may be involved in the HCC metastasis, but this still requires further mechanistic studies.
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