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31.
Chun-Yen Chen Chin-Yang Chang Hung-Jen Liu Ming-Huei Liao Chi-I Chang Jue-Liang Hsu Wen-Ling Shih 《Veterinary research》2010,41(2)
Our previous report demonstrated that bovine ephemeral fever virus (BEFV)-infected cultured cells could induce caspase-dependent apoptosis. This study aims to further elucidate how BEFV activates the caspase cascade in bovine cells. BEFV replicated and induced apoptosis in Vero and Madin-Darby bovine kidney (MDBK) cells, and a kinetic study showed a higher efficiency of replication and a greater apoptosis induction ability of BEFV in Vero cells. Src and c-Jun N-terminal kinase (JNK) inhibitor, but not extracellular signal-regulated kinase (ERK) or p38 inhibitor, alleviated BEFV-mediated cytopathic effect and apoptosis. In BEFV-infected Vero and MDBK cells, BEFV directly induced Src tyrosine-418 phosphorylation and JNK phosphorylation and kinase activity, which was inhibited specifically by SU6656 and SP600125, respectively. The caspase cascade and its downstream effectors, Poly (ADP-ribose) polymerase (PARP) and DFF45, were also activated simultaneously upon BEFV infection. In addition, cytochrome c, but not Smac/DIABLO, was released gradually from mitochondria after BEFV infection. SU6656 suppressed Src, JNK, and caspase-3 and -9 activation, as well as PARP and DFF45 cleavage; SP600125 reduced JNK and caspase-3 and -9 activation, as well as PARP and DFF45 cleavage. Taken together, these results strongly support the hypothesis that a Src-dependent JNK signaling pathway plays a key role in BEFV-induced apoptosis. The molecular mechanism identified in our study may provide useful information for the treatment of BEFV. 相似文献
32.
本试验以伊拉肉兔为研究对象,探究肉兔运输后在禁食与非禁食条件下对其应激水平、肉品质和行为的影响,探索合理的肉兔运输后的处理方式。试验选取80只体重相近（（2.5±0.5） kg）的伊拉公兔,随机分为8个组：对照组、运输后0 h组、非禁食6 h组、非禁食24 h、禁食6 h组、禁食24 h组、禁食行为观察组和非禁食行为观察组（做行为观察,不屠宰）。预试期为7 d,正式期的运输时间为2 h。结果发现,在血清生化测定中,和对照组相比,运输后0 h组血清ALT、AST、TG、Glu、CK、LDH水平无显著变化（P>0.05）,而运输后0 h组血清TP浓度显著下降,皮质醇浓度显著上升（P<0.05）。非禁食24 h组血糖水平高于禁食24 h组（P<0.05）、血清CK浓度低于禁食24 h组（P<0.01）,非禁食6 h的LDH水平低于禁食6 h组（P<0.05）。在肉品质测定中,运输后0 h时肌肉pH显著上升（P<0.05）,肌肉L*、a*水平显著下降（P<0.05）,而非禁食24 h组的L*、a*和b*值显著高于禁食24 h组。而禁食组与非禁食组的肌肉pH、失水率、蒸煮损失率和剪切力等无显著差异（P>0.05）。在基因表达方面,运输后0 h时JNK、Caspase-3的mRNA水平显著上升（P<0.05）。非禁食相比于禁食降低了JNK mRNA相对表达量（P<0.05）,对Caspase-3水平无显著影响（P>0.05）。在行为学方面,非禁食相比于禁食降低了肉兔的食粪行为（P<0.05）,对于肉兔刻板行为改变不明显（P>0.05）。本研究提示,在运输后静养期间,24 h非禁食能一定程度降低肉兔的应激、减少机体损伤、改善兔肉品质,有利于提高肉兔的福利水平。 相似文献
33.
Ching-Chyuan Su Jeff Yi-Fu Chen Zhong-Hao Din Jui-Hsin Su Zih-Yan Yang Yi-Jen Chen Robert Y.L. Wang Yu-Jen Wu 《Marine drugs》2014,12(10):5295-5315
13-acetoxysarcocrassolide (13-AC), an active compound isolated from cultured Formosa soft coral Sarcophyton crassocaule, was found to possess anti-proliferative and apoptosis-inducing activities against AGS (human gastric adenocarcinoma cells) gastric carcinoma cells. The anti-tumor effects of 13-AC were determined by MTT assay, colony formation assessment, cell wound-healing assay, TUNEL/4,6-Diamidino-2-phenylindole (DAPI) staining, Annexin V-fluorescein isothiocyanate/propidium iodide (PI) staining and flow cytometry. 13-AC inhibited the growth and migration of gastric carcinoma cells in a dose-dependent manner and induced both early and late apoptosis as assessed by flow cytometer analysis. 13-AC-induced apoptosis was confirmed through observation of a change in ΔΨm, up-regulated expression levels of Bax and Bad proteins, down-regulated expression levels of Bcl-2, Bcl-xl and Mcl-1 proteins, and the activation of caspase-3, caspase-9, p38 and JNK. Furthermore, inhibition of p38 and JNK activity by pretreatment with SB03580 (a p38-specific inhibitor) and SP600125 (a JNK-specific inhibitor) led to rescue of the cell cytotoxicity of 13-AC-treated AGS cells, indicating that the p38 and the JNK pathways are also involved in the 13-AC-induced cell apoptosis. Together, these results suggest that 13-AC induces cell apoptosis against gastric cancer cells through triggering of the mitochondrial-dependent apoptotic pathway as well as activation of the p38 and JNK pathways. 相似文献
34.
3-氯-1,2-丙二醇(3-MCPD)脂肪酸酯是一类在食品加工过程中产生的有害物质,关于其毒性机制尚不明确。本文以大鼠肾细胞NRK-52E为模型,采用RNA干扰技术,研究3-MCPD-1-棕榈酸单酯(C_(16:0)-ME)诱导肾细胞凋亡过程中JNK及p53的靶向调控作用,以及JNK1、JNK2和JNK3亚型在肾损伤过程中发挥的作用。结果表明,采用浓度为300μmol/L的C_(16:0)-ME处理细胞24h,JNK及p53磷酸化水平均显著提高,细胞凋亡相关蛋白bax及cleaved caspase-3表达量显著上调,bcl-2表达被明显抑制。当采用shRNA沉默p53蛋白表达后,采用浓度为300μmol/L的C_(16:0)-ME处理细胞24h,bax及cleaved caspase-3的表达均被抑制。在JNK 3个亚型中,只有JNK1shRNA处理组能显著减轻C_(16:0)-ME引起的肾细胞凋亡,p-c-Jun、bax、cleaved caspase-3、p53及p-p53的表达明显被抑制。研究结果表明,C_(16:0)-ME通过JNK1/p53通路诱导肾细胞凋亡。 相似文献
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AIM To observe the effect of Chaihu-Shugan decoction (CHSGD) on atherosclerosis in spontaneously hypertensive rats (SHR) and its possible mechanism. METHODS The male SHR (n =50) were randomly divided into model group (gavage of normal saline), compound kendir leaves (CKL) group (gavage of 0.5 g/kg CKL), and low-, medium- and high-dose CHSGD (CHSGD-L, CHSGD-M and CHSGD-H) groups (gavage of 2.5, 5 and 10 g/kg CHSGD, respectively), and another 10 male Wistar rats of the same origin were selected as normal control （NC) group (gavage of normal saline). The blood pressure was measured by intelligent noninvasive sphygmomanometer. The levels of blood lipids were measured by automatic biochemical analyzer. The expression of oxidative stress-related indexes, nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD), were detected by colorimetry. HE staining was used to detect the degree of atherosclerosis, and Western blot was used to detect the expression of Rho-associated kinase (ROCK)/c-Jun N-terminal kinase (JNK) signaling pathway-related proteins, RhoA, ROCK1 and JNK. RESULTS After 4 weeks of treatment, compared with NC group, the blood pressure, the serum levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and MDA, and the protein expression of RhoA, ROCK1 and JNK in aortic tissues of the rats in model group were significantly increased (P <0.05), and the serum levels of high-density lipoprotein cholesterol, NO and SOD were significantly decreased (P <0.05). HE staining showed that the diameter of aortas in the rats was thickened, a large number of foam cells were formed under the endothelium, and the proliferation of smooth muscle cells was observed. Compared with model group, the blood pressure, the serum levels of TG, TC, LDL-C and MDA, and the protein expression of RhoA, ROCK1 and JNK in aortic tissues of the rats in CKL, CHSGD-L, CHSGD-M and CHSGD-H groups were significantly decreased (P <0.05), and the serum levels of NO and SOD were significantly increased (P <0.05). HE staining showed that the structure of each layer of rat aortas gradually returned to normal, the vascular cells were in good order, and the inflammatory cell infiltration was slight. Compared with CKL group, the blood pressure, the serum levels of TG, TC, LDL-C and MDA, and the protein expression of RhoA, ROCK1 and JNK in aortic tissues of the rats in CHSGD-L and CHSGD-M groups were significantly increased (P <0.05), and the serum levels of NO and SOD were significantly decreased (P <0.05). No significant difference of the above indexes between CHSGD-H group and CKL group was observed (P >0.05). CONCLUSION Chaihu-Shugan decoction may attenuate the oxidative stress response via inhibition of ROCK/JNK signaling pathway, thus alleviating the symptoms of atherosclerosis in SHR. 相似文献
36.
【目的】 研究c-Jun氨基末端激酶(JNK)抑制剂SP600125对仔猪原代肝细胞药物性损伤的缓解作用及机理。【方法】 通过二步灌流法获得仔猪原代肝细胞，将肝细胞分为对照组(C)、JNK抑制剂组(SP)、模型组(M)和治疗组(T)，每组6个重复。对照组细胞不添加药物，SP组用2 μmol/L SP600125处理细胞，M组用80 μg/mL脂多糖(LPS)+20 μg/mL恩诺沙星(ENR)处理细胞，T组用80 μg/mL LPS+20 μg/mL ENR +2 μmol/L SP600125处理细胞，处理12 h后，收集上清测定谷丙转氨酶(ALT)和谷草转氨酶(AST)活性，收集细胞测定谷胱甘肽过氧化物酶(glutathione peroxidase，GSH-Px)、超氧化物歧化酶(superoxide dismutase，SOD)活性、丙二醛(malondialdehyde，MDA)含量及肝细胞核因子-1(hepatocyte nuclear factor 1，HNF-1)和谷胱甘肽-S-转移酶A1(glutathione S-transferase alpha 1，GSTA1)mRNA的相对表达量。【结果】 与对照组相比，M组肝细胞培养液上清中ALT和AST活性均显著升高(P<0.05)，M组肝细胞中GSH-Px和SOD活性、HNF-1和GSTA1 mRNA的相对表达量均极显著降低(P<0.01)，MDA含量极显著提高(P<0.01);与M组相比，T组肝细胞培养液上清中ALT、AST的活性均显著下降(P<0.05)，T组肝细胞中GSH-Px和SOD活性、HNF-1和GSTA1 mRNA的相对表达量均显著提高(P<0.05)，MDA含量显著降低(P<0.05)。【结论】 JNK抑制剂SP600125可通过调控细胞的抗氧化能力及HNF-1和GSTA1的表达缓解由LPS/ENR导致的仔猪原代肝细胞的药物性损伤。 相似文献