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ObjectiveTo explore the protective effect of Xielitang on ulcerative colitis （UC） mice induced by dextran sodium sulfate （DSS） and its possible mechanism. MethodSixty C57BL/6 mice were randomly divided into normal group， model group， sulfasalazine group and and low-， medium-， and high-dose Xielitang groups. Free drinking DSS solution to build the chronic UC model mice. Except for normal group， other groups were given 1.5% DSS for 3 cycles of drinking （days 1-7， days 22-28 and days 43-49） and distilled water for the rest of the time （days 8-21， days 29-42 and days 50-63）. After the first cycle， corresponding drugs were given for 42 days. The changes of general condition， body weight and disease activity index （DAI） score of mice were daily recorded during the experiment. At the end of the treatment， serum and colon tissue samples were collected， colon length was measured， intestinal weight index and colonic mucosal injury （CMDI） score were calculated. The pathological status of colon tissue was observed by hematoxylin-eosin （HE） staining. The levels of interleukin-6 （IL-6）， interleukin-10 （IL-10） and tumour necrosis factor-α （TNF-α） were measured by enzyme-linked immunosorbent assay （ELISA）. The gene and protein expressions of Toll like receptor 4 （TLR4）， nuclear transcription factor-κB （NF-κB） and hypoxia inducible factor-1α （HIF-1α） in colon tissue was detected by Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot. ResultCompared with the normal group， the body weight， colon length and IL-10 content in the model group were significantly decreased （P<0.01）， DAI score， intestinal weight index， CMDI score， IL-6 and TNF-α contents， and mRNA and protein expression levels of TLR4， NF-κB and HIF-1α in the model group were significantly increased （P<0.01）. Moreover， the structure of colonic mucosa was destroyed and inflammatory cells infiltrated in the model group. Compared with model group， body weight， colon length and IL-10 content in each dose group of Xielitang were significantly increased （P<0.05， P<0.01）， DAI score， intestinal weight index and CMDI score， IL-6 and TNF-α contents， mRNA and protein expression levels of TLR4， NF-κB and HIF-1α were notably decreased （P<0.05， P<0.01）. The pathological injury of colon was obviously alleviated. ConclusionXielitang can significantly improve the inflammatory response of UC mice induced by DSS， and its mechanism may be related to the regulation of TLR4/NF-κB/HIF-1α signaling pathway.
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Objective To explore the correlation between lipoprotein-associated phospholipase A2 (Lp-PLA2) and perioperative myocardial injury (PMI),and to discuss the predictive value of Lp-PLA2 in patients with stable angina after percutaneous coronary intervention (PCI).Methods A total of 222 consecutive patients with stable angina,who were admitted to Yixing Municipal People's Hospital,Jiangsu Province,China to receive PCI during the period from June 2015 to March 2017,were enrolled in this study.The patients' baseline data as well as the distribution pattern of coronary lesions,were recorded.According to the paclitaxel-PCI and the surgical cooperative study (SYNTAX) score,the severity of target vascular lesions was assessed,which was classified into low score group (0 to 22 points),middle score group (23 to 32 points) and high score group (≥33 points).The preoperative blood lipid level and renal function,both preoperative and postoperative Troponin T (cTnT),high sensitive C reactive protein(hs-CRP),as well as the postoperative Lp-PLA2 were tested.Results After the procedure,the Lp-PLA2 levels in patients with normal cTnT value (n=155) and in patients with elevated cTnT value (n=67) were(122.21±43.80) ng/ml and (224.53±65.00) ng/ml respectively (P＜0.05).SYNTAX score analysis showed that low score group had 120 patients,middle score group had 78 patients and high score group had 24 patients,the Lp-PLA2 levels of the above three groups were (119.51±51.96) ng/ml,(178.67±61.49) ng/ml and (233.16±61.32) ng/ml respectively,the differences were statistically significant between each other among the three groups (P＜0.05).Pearson correlation analysis indicated that a parallel correlation existed between Lp-PLA2 levels and postoperative cTnT values (R=0.492,P＜0.05).Logistic regression analysis revealed that Lp-PLA2 was the independent risk factor for elevated cTnT value during the perioperative period of PCI (OR=7.377,95％CI=3.368-16.156,P＜0.05).The area under ROC curve of Lp-PLA2 was 0.896 (95％CI=0.874-0.945,P＜0.001),the best cut-off point was 179 ng/ml,and the sensitivity and specificity for the diagnosis of PMI were 92.2％ and 66.7％,respectively.Conclusion Lp-PLA2 levels are closely correlated with the increased cTnT values after PCI,and the preoperative high level of Lp-PLA2 is the independent risk factor for PMI after PCI.
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<p><b>OBJECTIVE</b>To observe whether CD137 signaling could affect the nuclear factor of activated T cells c1 (NFATc1) expression through nuclear factor-κB (NF-κB) pathway in mice aortic vascular smooth muscle cells (VSMCs).</p><p><b>METHODS</b>Adherence methods for tissues explants were used for primary culture of mouse aortic VSMCs. The mRNA expression of CD137 and NFATc1 was detected by real-time quantitative PCR (RT-qPCR). The VSMCs protein expression of IκB-α, NF-κB p65, phospo-p65 and NFATc1 was determined by Western blot. The level of CD137 was measured by Flow Cytometry (FCM).</p><p><b>RESULTS</b>(1) The mRNA and protein expression of CD137 in VSMCs was significantly upregulated at 24 h after co-culture with TNF-α (10 ng/ml, all P < 0.05). (2) Compared with the control group, the level of p-NF-κB p65 in cytoplasm and nucleus was significantly increased (8.34 ± 0.28 vs. 1, P < 0.05, and 2.64 ± 0.42 vs. 1, P < 0.05) while the level of IκB-α was reduced (1 vs. 2.70 ± 0.28, P < 0.05) after co-treatment with agonist-CD137 mAb, above effects were partly blocked by adding specific NF-κB inhibitor PDTC (30 µmol/L: 1.15 ± 0.14 vs. 8.34 ± 0.28, P < 0.05, and 2.09 ± 0.12 vs. 2.64 ± 0.42, P < 0.05, and 1.78 ± 0.74 vs. 1, P < 0.05). (3) The mRNA (2.07 ± 0.09 vs. 1, P < 0.05) and protein (1.75 ± 0.07 vs. 1, P < 0.05) expression of NFATc1 was significantly upregulated by agonist CD137mAb compared with the control group, and these effects could be reversed by PDTC (1.15 ± 0.07 vs. 2.07 ± 0.09, P < 0.05, and 0.90 ± 0.11 vs. 1.75 ± 0.07, P < 0.05).</p><p><b>CONCLUSION</b>CD137 signaling could affect the NFATc1expression in VSMCs through NF-kappaB pathway.</p>