5μmol/L姜黄素)和对照组(正常台氏液培养120min代替模拟I/R),采用流式细胞术检测细胞凋亡情况,采用Western blot检测GSK-3、酪氨酸磷酸化GSK-3(pTyr-GSK-3)和丝氨酸磷酸化GSK-3(pSer-GSK-3)蛋白的表达。结果与对照组比较,模型组H9c2细胞凋亡率明显提高(t=10.439,P=0.000),模型组pTyr-GSK-3和pSer-GSK-3表达均显著增加(t=5.208,P=0.006;t=5.854,P=0.004)。与模型组比较,姜黄素组凋亡率及pTyr-GSK-3表达水平显著降低(t=-8.325,P=0.001;t=-3.607,P=0.023),存活率及pSer-GSK-3表达水平显著升高(t=9.165,P=0.001;t=3.747,P=0.02)。结论

GSK-3的酪氨酸和丝氨酸磷酸化可能参与心肌细胞I/R损伤,姜黄素减少I/R心肌细胞凋亡可能与其通过减少酪氨酸磷酸化、增加丝氨酸磷酸化抑制GSK-3活性有关。
锂剂是Mg2+的竞争性抑制剂,具有抗躁狂、抗抑郁、抗自杀的临床效果。锂剂有众多的直接目标分子,其中,锂剂通过抑制糖原合成酶激酶-3(GSK-3)发挥稳定情绪、改善行为、促进神经生长等作用。已有多项研究报道GSK-3参与神经变性性疾病、脑血管性疾病、神经系统肿瘤等疾病的发生,本文就GSK-3、锂剂和神经精神性疾病作一综述。
LPS刺激巨噬细胞产生IFN-β在抵御外来病原微生物的免疫反应中发挥重要作用。本研究探讨新抗生素S632A3促进LPS诱导巨噬细胞产生IFN-β及其分子机制。采用实时定量PCR检测mRNA含量,ELISA检测细胞因子含量,激酶分析检测GSK-3β活性,Western Autophagy inhibitor制造商 blotting检测蛋白磷酸化水平。结果表明:S632A3可显著促进LPS诱导的巨噬细胞产生IFN-β,其分子机制是抑制细胞内GSK-3β活性,降低转录因子c-Jun苏氨酸239位点的磷酸化并增加c-Jun稳定性。结果提示,S632A3是一个新的抗炎先导化合物,通过抑制GSK-3β活性促进LPS诱导巨噬细胞产生IFN-β。
Irradiation from diverse sources is ubiquitous and closely associated with human activities. Radiation therapy (RT), an important component of multiple radiation origins, is a common therapeutic modality for cancer. More importantly, RT provides significant

contribution to oncotherapy by killing tumor cells. However, during the course of therapy, irradiation of normal tissues can

result in a wide range of side effects, including self-limited acute toxicities, mild chronic symptoms, or severe organ dysfunction. 那个 Although numerous promising radioprotective agents have emerged, only a few have successfully entered the market because of various limitations. At present, the widely accepted hypothesis for protection against radiation-caused injury involves the Wnt canonical pathway. Activating the Wnt/β-catenin signaling pathway may protect the salivary gland, 获悉更多 oral mucosa, and gastrointestinal epithelium from radiation damage. The underlying mechanisms include inhibiting apoptosis and preserving normal tissue functions. However, aberrant Wnt signaling underlies a wide range of pathologies in humans, and its various components contribute to cancer. Moreover, studies have suggested that Wnt/ β-catenin signaling may lead to radioresistance of cancer stem cell. These facts markedly complicate any definition of the exact function of the Wnt pathway.
目的探讨Tau蛋白调控Fyn信号通路在阿尔茨海默病(AD)大鼠发病中的作用机制。方法雄性SD大鼠60只随机分为正常组,模型组及观察组。采用β淀粉样蛋白毒性片段(Aβ25～35)海马注射制备AD大鼠模型。10μmol/L SB216763(Tau蛋白抑制剂)注射至观察组大鼠脑组织。采用SABC法对大鼠脑组织中Tau蛋白进行免疫组化检测,Western印迹检测Fyn和Fak的表达。结果与正常组相比,模型组大鼠脑组织Tau蛋白含量及Fyn和Fak的表达显著增加(P<0.