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Conclusion TSCC patients with low expression of PTEN and high expression of STING have poor prognosis and short survival time. Combined detection of PTEN and STING expression is helpful to evaluate the degree of tumor progression and patient prognosis.Objective To investigate the role and mechanism of endothelin receptor antagonist CPU0213 in myocardial ischemia-reperfusion (I/R) injury and oxidative stress injury. Methods In order to investigate the role of CPU0213 in I/R, SD rats were randomly divided into sham operation group, ischemia reperfusion injury (I/R) group, CPU0213 treatment group after I/R, CPU0213 and Janus kinase 2 (JAK2) specific inhibitor AG490 treatment group after I/R. In order to investigate the role of CPU0213 in oxidative stress damage, the isolated and characterized cardiomyocytes were cultured and divided into control group, H2O2 oxidative stress group (H2O2 group), oxidative stress damaged group treated with CPU0213, and oxidative stress damaged group treated with CPU0213 and AG490. The rat myocardial I/R models were constructed, and the rats and cardiomyocytes were treated with different treatments according to the experimental requirements. The rat heart was stained with triphenyltetrazolium chloride (TTC) to observe the area ofncreased, Bcl2 expression dropped significantly, cell viability decreased significantly. Conclusion The activation of JAK2/STAT3 pathway by CPU0213 can inhibit the apoptosis of cardiomyocytes induced by I/R and oxidative stress.Objective To explore the effects of D-galactose (D-gal) on barrier function of murine TM4 sertoli cells and its mechanism. Methods TM4 cells were divided into control group and 25, 50, 100, 150, 200, 250 mmol/L D-gal stimulation group. The viability of TM4 cells was determined by MTT assay. The protein expression levels of tight junction-related proteins including zonula occluden-1 (ZO-1) and occludin, adheren junction-related proteins including neural cadherin (N-cadherin), epithelial cadherin (E-cadherin) and β-catenin, gap junction-related protein connexin43 (CX43) and cytoskeleton-related protein vimentin, and MAPK signaling pathway-related proteins ERK1/2, phosphorylated ERK1/2 (p-ERK1/2), JNK, phosphorylated JNK (p-JNK), p38MAPK and phosphorylated p38MAPK (p-p38MAPK) were detected by Western blot analysis. Results Compared with the control group, the viability of TM4 cells significantly decreased when the concentration of D-gal was more than 50 mmol/L. In addition, the protein expression levels of ZO-1, occludin, N-cadherin, E-cadherin and β-catenin were significantly down-regulated in D-gal-treated group, while the protein expression levels of p-p38MAPK were significantly up-regulated. However, there were no differences in the protein expression levels of CX43, vimentin, p-ERK, ERK1/2, p-JNK and JNK between the control group and D-gal-treated groups. https://www.selleckchem.com/products/mrtx0902.html Conclusion D-gal can disrupt tight junction and adheren junction of TM4 cells via the activation of p38MAPK signaling pathway.Objective To investigate the role of butorphanol in alleviating ischemic arrhythmias and its regulatory effects on the microRNA-1-3p/connexin 43 (miR-1-3p/Cx43) pathway. Methods SD rats were divided into the following groups control group (the treatment was the same as that of modeling, but no coronary artery ligation was performed), butorphanol group (rats were injected 50 μg/kg butorphanol into the femoral vein after the needle has penetrated the myocardial surface), inhibitor group (5 days before the experiment, 80 mg/kg miR-1-3p inhibitor was administered via the tail vein, and the other treatment were the same as the control group); model group (ligation method was used to prepare rat ischemic arrhythmia models), butorphanol pretreatment group (50 μg/kg butorphanol was given at 5 minutes before ischemic treatment, and the other treatment were the same as the model group), inhibitor pretreatment group (5 days before the experiment, 80 mg/kg miR-1-3p inhibitor was administered via the tail vein, and the otdecreased the total score of ventricular arrhythmia in the rats with ischemic arrhythmia, and significantly increased the expression of Cx43 mRNA and protein. Conclusion Butorphanol can improve ischemic arrhythmia by up-regulating the expression of Cx43 mediated by miR-1-3p.Objective To investigate the effects of miR-23b-3p on proliferation, migration and invasion of human cervical carcinoma CasKi cells. Methods Human cervical carcinoma CasKi cells and normal epithelial HaCaT cells were cultured in vitro. Real-time quantitative RT-PCR was conducted to detect the expression of miR-23b-3p in CasKi and HaCaT cells. Synthetic miR-23b-3p mimic and its negative control were transfected into CasKi cells by liposome method. The effects of miR-23b-3p over-expression on cell proliferation were detected by CCK-8 assay. Wound scratch healing assay and TranswellTM assay were used to observe the migration and invasion abilities of CasKi cells, respectively. Western blot analysis was used to detect the protein expression of N-cadherin, vimentin, E-cadherin, Snail, PCNA and cyclin D1. Results The expression of miR-23b-3p in CasKi cells was lower than that of HaCaT cells. Compared with the negative control group, the expression of miR-23b-3p were significantly up-regulated in CasKi cells after transfected with miR-23b-3p mimic. CCK-8 and Western blot assays showed that the proliferation was inhibited and the expression of PCNA and cyclin D1 were down-regulated after the cells were treated with miR-23b-3p mimic. At the same time, after over-expression of miR-23b-3p, the migration and invasion abilities of the CasKi cells were significantly inhibited. In addition, the expression of E-cadherin was up-regulated, while vimentin, Snail and N-cadherin expression levels were significantly down-regulated. Conclusion Over-expression of miR-23b-3p may suppress the proliferation, migration, invasion and epithelial-mesenchymal transition process of human cervical cancer CasKi cells.Objective To observe the effect of acute severe air pollution exposure on cytokines and chemokines in lung tissues of rats and explore its significance. Methods During the period of severe air pollution in Beijing from December 17 to 22, 2016, rats were exposed to air pollution for 6 days, and then sacrificed on the 7th day. Lung tissues were taken and their histological changes were observed by HE staining. The levels of 22 cytokines/chemokines in the lung tissue homogenate supernatant were detected by liquid chip method. Results Compared with the control group, the lung tissues of the rats in the air pollution exposure group were characterized by widened alveolar septum, inflammatory cell infiltration and vascular bleeding. Chemokines eotaxin, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), regulated on activation, normal T cell expressed and secreted factor (RANTES), and proinflammatory cytokines interleukin 1β (IL-1β), IL-17, IL-18, tumor necrosis factor α (TNF-α) in the supernatant of lung homogenate of rats in the air pollution exposure group significantly increased.

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