ABSTRACT
Objective:To investigate the relationship between manganese superoxide dismutase (MnSOD) gene Val16Ala polymorphism and the susceptibility to prostate cancer.Methods:All literatures related to MnSOD gene polymorphism and susceptibility to prostate cancer were retrieved from PubMed, Embase, China Knowledge Network and Wanfang databases. The retrieval time was from the database establishment to September 19, 2018. Literature screening and data extraction were independently done by 2 investigators, and Meta-analysis was performed by using Stata 12.0 software.Results:A total of 17 studies were included in the final analysis, including 7 101 prostate cancer cases and 9 146 healthy controls (people working at hospital and the ordinary people). The results of Meta-analysis showed that MnSOD gene Val16Ala polymorphism was not associated with susceptibility to prostate cancer under the homozygous model ( OR = 1.12, 95% CI 1.02-1.23, P = 0.435), heterozygous model ( OR = 1.14, 95% CI 1.05-1.24, P = 0.765), dominant model ( OR = 1.14, 95% CI 1.05-1.23, P = 0.552) and allele comparison model ( OR = 1.07, 95% CI 1.02-1.12, P = 0.106). Conclusion:There may not be the relationship between MnSOD gene Val16Ala polymorphism and the susceptibility to prostate cancer.
ABSTRACT
Objective To investigate the protective effects of Erqi Decoction(EQD; mainly composed of Radix Aristolochiae Kaempferi, Radix Rhizoma Seu Flos Cypripedii, Cortex Fraxini, Cortex Phellodendri, Radix et Rhizoma Rhei) on the intestinal tract in rats with acute radiation intestinal injury and its mechanism. Methods Sixty SD rats were randomly divided into normal group, model group, EQD group and Baitouweng Decoction group (BD group), 15 rats in each group. The acute radiation enteritis model was established by exposing the whole abdomen to a total dose of 10 Gy of 6 MV higher-energy X-rays. EQD group and BD group were given intragastrical administration with corresponding medicine of EQD at the dose of 8.85 g·kg-1·d-1, BD at the dose of 4.69 g·kg-1·d-1 respectively, and the normal group and the model group were given intragastrical administration with the same volume of normal saline. The treatment lasted for 7 continuous days. After modeling, the morphological change of the proximal ileum tissue was observed under light microscope. Villus height, crypt depth, and thickness of the ileal mucosa and entire wall were measured by image analysis system. The myeloperoxidase (MPO) content in ileum tissue was determined by spectrophotometer, and the expression levels of caspase -3 and proliferating cell nuclear antigen (PCNA) in ileum tissue were determined by immunohistochemistry. Results EQD group and BD group had milder injuries of the ileal structure, and had higher villus height, crypt depth, and thickness of mucosa and entire wall than those in the model group (P 0.05). MPO content in EQD group and BD group was decreased(P0.05). Conclusion EQD has certain protective effects against radiation-induced intestinal damage, which mechanism is probably associated with relieving the local intestinal inflammatory reaction, accelerating intestinal epithelial cell proliferation, and inhibiting intestinal epithelial cell apoptosis.
ABSTRACT
Objective To investigate the effects of IL-10/TGF-β-modified macrophages on renal ischemia reperfusion injury (IRI).Methods Bone marrow-derived macrophages were modified ex vivo by IL-10/TGF-β to acquire M2c (a subset of activated macrophages).M2c were transferred into treated C57BL/6 mice by a single tail-vein injection at 6 h after renal IRI.Mice were killed on the day 3 after renal IRI.Blood samples were collected to check renal function.Kidneys were harvested to determine tubular necrosis and apoptosis by H&E staining and TUNEL assay.Immunofluorescence was performed to analyze the proliferating tubular cell nuclear antigen.Meanwhile,proinflammatory cytokines and regulatory T cells in renal tissues were analyzed with real-time PCR and flow cytometry.Results In comparison with M1,M2c expressed lower levels of MHC Ⅱ (P＜0.01),CD86 (P＜ 0.01),TNFα (P＜0.01) and IL-1β (P＜0.01) and higher level of IL-10 (P＜0.01).M2c significantly attenuated renal functional decline (P＜0.01 or 0.05),structural injury (P＜0.05),apoptosis of tubular cells (P＜0.01) and inflammation factors infiltration (P＜0.01 or 0.05).What's more,the cells could promote tubular cells proliferation (P＜0.05) and regulatory T cells expression (P＜0.01).Conclusion Our results demonstrated that M2c macrophages effectively protect against renal IRI and may become a therapeutic strategy for renal IRI.