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金太伟;高小宁;宋文琳;王妍妍;孙琳;陆玲红 《电波科学学报》2024,59(6):1639-1646
本研究旨在探讨苏木酮A (sappanone A, SA) 调控大鼠肾脏缺血再灌注损伤(ischemia-reperfusion injury, IRI) 的作用和机制。动物实验已获得苏州市吴江区儿童医院伦理委员会批准(批准号: 2022010)。首先利用苏木精-伊红染色法(hematoxylin-eosin staining, H&E) 观察大鼠肾组织形态学变化并进行肾损伤评分; 提取血清检测肌酐(serum creatinine, SCr)、尿素氮(blood urea nitrogen, BUN) 和胱抑素C (cystatin C, Cys C) 的含量; 通过TUNEL染色进一步分析苏木酮A对IRI引起的肾小管上皮细胞凋亡情况的影响; 免疫印迹法(Western blot) 检测肾组织中p-JNK/JNK、p-ERK/ERK、Bcl2、Bax和cleaved-caspase 3的蛋白表达水平。最后, 通过以上研究方法明确JNK激活剂茴香霉素(anisomycin, Ani) 是否可以逆转苏木酮A对大鼠IRI的保护作用。结果显示, 苏木酮A明显减轻IRI引起的肾小管损伤, 减少血清中SCr、BUN和Cys C的含量。TUNEL染色显示, 苏木酮A明显减少IRI引起的肾小管上皮细胞凋亡。Western blot检测肾组织表明, 苏木酮A明显促进凋亡抑制蛋白Bcl2的表达, 抑制凋亡促进蛋白Bax和cleaved-caspase 3的表达, 进一步分析显示苏木酮A不影响ERK的磷酸化, 而抑制JNK的磷酸化。最后, 通过H&E染色、血清学检测、TUNEL染色和免疫印迹法证实JNK激活剂茴香霉素可以逆转苏木酮A对大鼠IRI的保护作用。上述研究结果表明, 苏木酮A通过抑制JNK磷酸化减轻大鼠肾脏缺血再灌注损伤。 相似文献
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Nu Ry Song Hee Yang Jiman Park Jung Yeon Kwon Nam Joo Kang Yong Seok Heo Ki Won Lee Hyong Joo Lee 《Food chemistry》2012
Cyanidin, an anthocyanidin found in fruits and vegetables, has been reported to possess anti-cancer effects. However, there is no study on the chemopreventive effect of cyanidin against neoplastic cell transformation and its molecular mechanisms. In the present study, we compare the anti-carcinogenic effects of cyanidin and cyanidin-3-glucoside (C3G) and investigate their underlying mechanisms. The inhibitory effect of cyanidin on EGF-induced cell transformation was higher than those of C3G in JB6 P+ mouse epidermal (JB6 P+) cells. Both cyanidin and C3G showed dose-dependent radical scavenging activities. It is indicated that the divergent inhibitory effects of cyanidin and C3G are not due to their antioxidant activities. We found that cyanidin, but not C3G, inhibited the EGF-induced Akt/p70S6K phosphorylation. Moreover, cyanidin directly suppressed the activity of PI3K by binding to PI3K directly in an ATP-competitive manner, which indicates that PI3K is one of the molecular targets of cyanidin. 相似文献
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目的: 观察抗血小板溶栓素(anti-platelet thrombolysin,APT)对缺血性脑损伤的保护作用并初步探讨其作用机制。方法: SD大鼠,随机分为假手术组(Sham)、模型组(缺血再灌注组)、阳性组(依达拉奉注射液)、APT高、中、低组。双侧颈动脉结扎,建立脑缺血模型,测定大鼠脑含水量,HE染色观察脑组织病理改变;线栓法建立大鼠脑缺血/再灌注模型,进行行为学评分,酶联免疫法(ELISA)及免疫组化测定脑组织中Toll样受体4(TLR4)、c-Jun氨基末端激酶(JNK)、Bax蛋白含量。结果: 与模型组比较,APT高、中剂量组可明显改善缺血再灌注后大鼠神经功能障碍症状,降低脑水肿程度,改善缺血后脑组织的病理改变,明显降低缺血后脑组织中TLR4、JNK、Bax蛋白表达。结论: APT对缺血性脑损伤有较好的保护作用,其机制可能与抑制脑组织中TLR4/JNK/Bax信号通路表达,从而抑制细胞凋亡有关。 相似文献
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Cheng-Chin Huang Ching-Yao Yang Chin-Chuan Su Kai-Min Fang Cheng-Chieh Yen Ching-Ting Lin Jui-Min Liu Kuan-I Lee Ya-Wen Chen Shing-Hwa Liu Chun-Fa Huang 《International journal of molecular sciences》2021,22(9)
4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP), a major active metabolite of bisphenol A (BPA), is generated in the mammalian liver. Some studies have suggested that MBP exerts greater toxicity than BPA. However, the mechanism underlying MBP-induced pancreatic β-cell cytotoxicity remains largely unclear. This study demonstrated the cytotoxicity of MBP in pancreatic β-cells and elucidated the cellular mechanism involved in MBP-induced β-cell death. Our results showed that MBP exposure significantly reduced cell viability, caused insulin secretion dysfunction, and induced apoptotic events including increased caspase-3 activity and the expression of active forms of caspase-3/-7/-9 and PARP protein. In addition, MBP triggered endoplasmic reticulum (ER) stress, as indicated by the upregulation of GRP 78, CHOP, and cleaved caspase-12 proteins. Pretreatment with 4-phenylbutyric acid (4-PBA; a pharmacological inhibitor of ER stress) markedly reversed MBP-induced ER stress and apoptosis-related signals. Furthermore, exposure to MBP significantly induced the protein phosphorylation of JNK and AMP-activated protein kinase (AMPK)α. Pretreatment of β-cells with pharmacological inhibitors for JNK (SP600125) and AMPK (compound C), respectively, effectively abrogated the MBP-induced apoptosis-related signals. Both JNK and AMPK inhibitors also suppressed the MBP-induced activation of JNK and AMPKα and of each other. In conclusion, these findings suggest that MBP exposure exerts cytotoxicity on β-cells via the interdependent activation of JNK and AMPKα, which regulates the downstream apoptotic signaling pathway. 相似文献
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为研究不同提取方法的灵芝多糖(GLP)对脂多糖(LPS)诱导的RAW264.7细胞体外抗炎活性,以回流提取、复合酶法提取、植物乳杆菌发酵+回流提取、植物乳杆菌发酵+复合酶法提取4种方法提取GLP。以LPS诱导建立RAW264.7细胞炎症模型,加入GLP处理24 h,采用CCK-8法检测GLP对RAW264.7细胞生存率的影响,实时荧光定量PCR(qRT-PCR)法检测炎症细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、诱导型一氧化氮合酶(iNOS)的mRNA表达水平,免疫印迹检测JNK/P38 MAPK信号通路蛋白的表达。结果表明:质量浓度在200 μg/mL及以下的4种GLP作用于RAW264.7细胞时,细胞存活率为93%以上。与LPS相比,4种方法提取的GLP均可显著(P＜0.05)影响RAW264.7细胞炎症因子TNF-α、IL-6、IL-10、iNOS的mRNA表达水平。与回流提取GLP相比,植物乳杆菌发酵+回流提取GLP可显著(P＜0.05)抑制TNF-α、IL-6的mRNA表达及促进IL-10的mRNA表达。与另外3种方法提取GLP相比,植物乳杆菌发酵+复合酶法提取GLP可显著(P＜0.05)抑制iNOS的mRNA表达水平。与回流提取和复合酶法提取GLP相比,经植物乳杆菌发酵后提取的2种GLP,均能显著(P＜0.05)降低P-JNK、P-P38的蛋白表达。GLP具有较好的体外抗炎活性,不同提取方法对GLP体外抗炎活性的影响较大,其中植物乳杆菌发酵后提取的GLP具有更显著的抗炎活性。 相似文献
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A functional comparison of three human SAPKs with fungal Hog1p was undertaken, using Saccharomyces cerevisiae as a heterologous expression system. We characterized the role of mammalian MAP kinases in sensitivity to both osmotic and oxidative stress of a S. cerevisiae hog1 mutant. Western blot analyses indicated that S. cerevisiae can only phosphorylate mammalian MAP kinases in response to osmotic stress but not to oxidative stress, while morphogenetic defects characteristic of hog1 mutants under hyperosmotic stress are only suppressed by fungal and not mammalian Hog1p. Our data demonstrate the functional conservation of MAPKs although they also evidence differential aspects among the three human SAPKs and the fungal MAPKs. 相似文献
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目的: 探讨C-Jun氨基末端激酶(JNK)在缺血后处理(IPO)减轻缺血/再灌注损伤大鼠肺细胞凋亡中的作用。方法: 雄性SD大鼠随机分成5组(n＝8),即对照组(C组)、肺缺血/再灌注组(I/R组)、肺缺血/再灌注+缺血后处理组(IPO组)、缺血后处理+溶剂对照组(PPCES溶液)(P组)、缺血后处理+SP600125组(SP组)。分别于再灌注 2 h 颈动脉取血、留取左肺组织,检测血清超氧化物歧化酶(SOD)、丙二醛(MDA)、髓过氧化物酶(MPO),检测肺组织湿/干重比(W/D)和总肺含水量(TLW);光电镜观察肺组织形态学结构改变,并进行肺组织损伤定量评估(IQA);原位末端标记法(TUNEL)检测肺细胞凋亡情况并计算凋亡指数(AI)。结果: 与C组相比,I/R组血清SOD活性显著降低,MDA含量、MPO活力显著升高(P均<0.01),肺组织W/D、TLW、IQA和AI均显著升高(P<0.05 或P<0.01),光镜电镜下肺组织结构发生明显损伤;IPO组、P组、SP组与I/R组相比,MDA含量、MPO活力显著降低,SOD活性升高(P<0.05 或P<0.01),肺组织W/D、TLW、IQA和AI均显著降低(P<0.05 或P<0.01),光镜电镜下肺组织结构损伤情况有所改善;P组与IPO组比较各项指标均无明显差异(P均>0.05);SP组与IPO组相比,MDA含量、MPO活力显著降低,SOD活性升高(P<0.05 或P<0.01),肺组织W/D、TLW、IQA和AI均显著降低(P<0.05或P<0.01),光镜电镜下肺组织结构未见明显损伤。结论: I/R导致大鼠肺组织过度氧化应激,激活JNK,肺内中性粒细胞聚集,导致肺组织结构严重破坏,细胞大量凋亡;IPO可以减轻氧化应激,抑制JNK通路的激活,从而改善其结构破坏和细胞凋亡。 相似文献
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