摘要：
The present study aimed to investigate the effect of hydrogen sulfide (H2S) on kidney injury induced by urinary-derived sepsis. Rabbits were randomly divided into control, sham, sepsis, NaHS 2.8 mumol/kg and NaHS 8.4 mumol/kg groups, with six rabbits in each group. Upper urinary tract obstruction and acute infection was induced to establish the sepsis model. Blood was collected to carry out a white blood cell (WBC) count, and creatinine (Cr) and blood urea nitrogen (BUN) analysis. Morphological changes were observed by hematoxylin and eosin (H&E) staining and transmission electron microscopy. Immunohistochemical staining was used to detect the expression levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-10 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB). Cystathionine-gamma-lyase (CSE) activity was measured by the spectrophotometric methylene blue method and the blood H2S concentration was measured by deproteinization. WBC, Cr and BUN levels were significantly elevated in the sepsis group compared with those in the control group (P<0.05). Following treatment with NaHS, the WBC, Cr and BUN levels were significantly decreased in the NaHS groups compared with those in the sepsis group (P<0.05). The pathological features of kidney injury were also alleviated by NaHS. In the sepsis group, the levels of TNF-alpha, IL-10 and NF-kappaB were significantly increased compared with those in the control group (P<0.05). In the NaHS groups, the TNF-alpha and NF-kappaB levels were significantly reduced whereas the IL-10 level was significantly increased compared with the respective levels in the sepsis group (P<0.05). The H2S concentration was significantly decreased in the sepsis group and this reduction was attenuated in the NaHS groups (P<0.05). Furthermore, the NaHS 8.4 mumol/kg dose revealed a more potent effect than the NaHS 2.8 mumol/kg dose. Thus, exogenous H2S reduced kidney injury from urinary-derived sepsis by decreasing the levels of NF-kappaB and TNF-alpha, and increasing the level of IL-10.
期刊：
EXPERIMENTAL AND THERAPEUTIC MEDICINE,2014年8(1):3-8 ISSN：1792-0981
通讯作者：
Qin, Li
作者机构：
[Guo, Qiong; Zhu, Neng; Yang, Luoyan] Cent S Univ, Xiangya Hosp 2, Dept Urol, Changsha 410011, Hunan, Peoples R China.;[Luo, Zhigang; Zhu, Neng] South China Univ, Affiliated Hosp 2, Dept Urol, Hengyang 421001, Hunan, Peoples R China.;[Qin, Li] Univ South China, Inst Pharm & Pharmacol, Hengyang 421001, Hunan, Peoples R China.;[Liao, Duanfang; Qin, Li] Hunan Univ Chinese Med, Sch Pharm, Changsha 410208, Hunan, Peoples R China.;[Qin, Li] Univ South China, Inst Pharm & Pharmacol, 28 Changsheng West Rd, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Qin, Li] U;Univ South China, Inst Pharm & Pharmacol, 28 Changsheng West Rd, Hengyang 421001, Hunan, Peoples R China.
关键词：
Wnt5a;cancer;metastasis;signaling pathway
摘要：
Wnt5a is a noncanonical signaling member of the wingless-related/mouse mammary tumor virus integration family, which is involved in a wide range of cellular processes, particularly in cancer development and metastasis. Accumulating evidence indicates that Wnt5a exhibits paradoxical effects in various types of cancer metastasis. Therefore, the Wnt5a signaling cascade in cancer metastasis appears to be complex and may depend on binding receptors, downstream effectors, exogenous inhibitors and tumor microenvironments, as well as the extracellular matrix, particularly cell/tissue-tropic contexts. The aim of the present study was to summarize the previous findings on the roles of Wnt5a and the potential mechanisms in various types of cancer metastasis. Furthermore, it is reasonable to hypothesize that Wnt5a and the involved signaling pathways may become molecular targets in the treatment of cancer metastasis.
