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Peng L.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | Li J.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | Xu Y.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | Wang Y.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | And 3 more authors.
International Journal of Endocrinology | Year: 2016

Background. p38 mitogen-activated protein kinase (MAPK) plays a crucial role in regulating signaling pathways implicated in inflammatory processes leading to diabetic nephropathy (DN). This study aimed to examine p38 MAPK activation in DN and determine whether beraprost sodium (BPS) ameliorates DN by inhibiting inflammation and p38 MAPK signaling pathway in diabetic rats. Methods. Forty male Sprague Dawley (SD) rats were randomly divided into the normal control group, type 2 diabetic group, and BPS treatment group. At the end of the 8-week experiment, we measured renal pathological changes and the activation of the p38 MAPK signaling pathway and inflammation. Result. After BPS treatment, renal function, 24-hour urine protein, lipid profiles, and blood glucose level were improved significantly; meanwhile, inflammation and the expression of p38 MAPK signaling pathway in the diabetic kidney were attenuated. Conclusions. BPS significantly prevented type 2 diabetes induced kidney injury characterized by renal dysfunction and pathological changes. The protective mechanisms are complicated but may be mainly attributed to the inhibition of the p38 MAPK signaling pathway and inflammation in the diabetic kidney. © 2016 Li Peng et al. Source


Li J.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | Wang H.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | Hang C.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | Fan Y.,Nanjing General Hospital of Nanjing Military Command Jinling Hospital | And 2 more authors.
Applied Biochemistry and Biotechnology | Year: 2015

Tectonic-1, also named as TCTN1 or TECT1, which belongs to a family of signal-sequence-containing secreted and transmembrane proteins evolutionarily conserved among eukaryotes, was reported to be involved in central nervous system development and ciliogenesis. In this paper, we found that TCTN1 is extensively expressed in human glioma cell lines. To clarify the role of TCTN1 in glioma, we employed lentivirus-mediated short hairpin RNA to knock down TCTN1 expression in U251 and U87MG glioma cells. Knockdown of TCTN1 potently inhibited cell proliferation, as determined by MTT and colony formation assays. Cell cycle analysis showed depletion of TCTN1 led to both U251 and U87MG cells arrested in the G0/G1 phase. These data suggest TCTN1 is essential for glioma cell viability, and dysregulation of TCTN1 may play a key role in glioma tumorigenesis. © 2015, Springer Science+Business Media New York. Source

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