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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Cell Line,Hypoxia-Reoxygenation,Nec-1,Necrosome,Receptor interacting protein
- چکیده:
- چکیده انگلیسی: Objective(s): The aim of this study is to explore the potential role of hypoxia/reoxygenation in necroptosis in cultured rat renal tubular epithelial cell line NRK-52E, and further to investigate its possible mechanisms.
Materials and Methods: Cells were cultured under different hypoxia-reoxygenation conditions in vitro. MTT assay was used to measure the cell proliferation of cells that were exposed to hypoxia-reoxygenation conditions at different time points. Receptor-interacting protein 1,3 (RIP1 and RIP3) and NF-κB were detected by Western-blot analysis. Co-immunoprecipitation (Co-IP) was conducted to investigate the formation of necrosome. Necrostatin-1 (Nec-1) was adopted to inhibit the occurrence of necroptosis. In addition, morphological changes of cells after hypoxia-reoxygenation interference were observed under transmission electron microscope (TEM).
Results: MTT assay indicated that hypoxia-reoxygenation treatment can cause a decrease in cell viability. Particularly, 6 hr of hypoxia and 24 hr of reoxygenation (H6R24 group) resulted in the lowest cell viability. Western-blot results indicated that the expression of RIP3 significantly increased in H6R24 group while the expression of NF-κB is decreased. Co-IP results demonstrated that the interaction between RIP1 and RIP3 was stronger in the hypoxia-reoxygenation induced group than the other groups, furthermore, treatment with Nec-1 reduced the formation of necrosome. TEM observation results showed that hypoxia-reoxygenation treated cells showed typical morphological characteristics of necroptosis and autophagy.
Conclusion: Hypoxia-reoxygenation treatment can induce necroptosis in NRK-52E cells, and this effect can be inhibited by Nec-1. In addition, the mechanism of necroptosis induced by hypoxia-reoxygenation injury on cells may be related to the low expression of NF-κB.- انتشار مقاله: 22-06-1396
- نویسندگان: Changlai Zhu,Yang Liu,Zongyu Guan,Yi Zhou,Fang Liu,Tianyi Zhang
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Inflammation,Diabetic nephropathy,Herb,Renal injury
- چکیده:
- چکیده انگلیسی: Objective(s): It has been widely reported that Mori cortex extract (MCE) is used for the treatment of diabetes mellitus in traditional medicine. The present study was designed to investigate its mechanism of action in the treatment of diabetic nephropathy (DN). We assessed whether MCE preventive treatment ameliorates kidney damage in high-fat diet and streptozotocin (STZ)-induced type 2 diabetic rats.
Materials and Methods: Rats were fed a high-fat diet and injected with STZ. MCE was given to rats daily at 10 g/kg. Fasting blood glucose (FBG) and postprandial plasma glucose were measured. Blood and urine biochemical parameters, renal tissue morphology, and inflammation were investigated.
Results: Prevention with MCE significantly decreased FBG and homoeostasis model assessment (HOMA) of IR (HOMA-IR) levels and increased insulin levels in diabetic rats. MCE prevention significantly decreased levels of KW/BW, BUN, Cr, and 24 hr urinary protein. MCE inhibited glomerular basement membrane thickening, tubular epithelial cell hypertrophy, and glomerular capillary dilation. MCE also prevented the disappearance of bowman’s space and renal tubular lumen and decreased collagen deposition in rat kidney. Moreover, MCE reduced the levels of inflammatory factors (MCP-1 and TNF-α) and fibrosis factors (collagen IV and fibronectin).
Conclusion: MCE prevents DN through inhibition of inflammation and fibrosis in a rat model. It might provide a safe and effective way to prevent DN.- انتشار مقاله: 13-03-1396
- نویسندگان: Lili Ma,Hailai Ni,Xinrong Zou,Yanyan Yuan,Chun Luo,Bingyang Liu,Fuyan Wang,Yang Xi,Yudong Chu,Pangjie Xu,Xiaohui Qiu,Song Li,Shizhong Bu
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Bioinformatics analysis,Ovarian Cancer,Microarray,Diabetes Mellitus
- چکیده:
- چکیده انگلیسی: Ovarian cancer is one of the three major gynecologic cancers in the world. The aim of this study is to find the
relationship between ovarian cancer and diabetes mellitus by using the genetic screening technique. By GEO database
query and related online tools of analysis, we analyzed 185 cases of ovarian cancer and 10 control samples from
GSE26712, and a total of 379 different genes were identified, including 104 up-regulated genes and 275 down-regulated
genes. The up-regulated genes were mainly enriched in biological processes, including cell adhesion, transcription of
nucleic acid and biosynthesis, and negative regulation of cell metabolism. The down-regulated genes were enriched in
cell proliferation, migration, angiogenesis and macromolecular metabolism. Protein-protein interaction was analyzed
by network diagram and module synthesis analysis. The top ten hub genes (CDC20, H2AFX, ENO1, ACTB, ISG15,
KAT2B, HNRNPD, YWHAE, GJA1 and CAV1) were identified, which play important roles in critical signaling
pathways that regulate the process of oxidation-reduction reaction and carboxylic acid metabolism. CTD analysis
showed that the hub genes were involved in 1,128 distinct diseases (bonferroni-corrected P<0.05). Further analysis by
drawing the Kaplan-Meier survival curve indicated that CDC20 and ISG15 were statistically significant (P<0.05). In
conclusion, glycometabolism was related to ovarian cancer and genes and proteins in glycometabolism could serve as
potential targets in ovarian cancer treatment.- انتشار مقاله: 04-04-1397
- نویسندگان: Yi Sun,Huang Xiaoyan,Liu Yun,Liu Chaoqun,Wen Jialing,Yang Liu,Zhao Yingqi,Yi Peipei,Peng Junjun,Lu Yuanming
- مشاهده