第二个线粒体衍生半胱天冬氨酸蛋白酶激活剂(second mitochondria‐derived activator of caspase,Smac){3}是一类存在于线粒体中的凋亡抑制{3}(inhibitor of apoptosis protein,IAP)拮抗剂,在肿瘤细胞凋亡过程中从线粒体释放,与IAP结合抑制其功能。目前Smac模拟物已经成为癌症中一类很有前途的靶向疗法,正在进行临床测试。乳腺癌作为全球女性最常见的癌症,其治疗受到广泛关注。本文针对Smac模拟物在乳腺癌治疗中的相关研究进展作一综述。
目的探讨第二个线粒体衍生半胱天冬氨酸蛋白酶激活剂(Smac)、催乳素(PRL)在子宫内膜异位症中的应用价值。方法选取2018年1月-2019年12月在丽水市中心医院治疗的子宫内膜异位症患者80例(观察组),同时选取健康志愿者80例作为对照组,检测血清Smac、PRL水平及子宫内膜厚度。结果观察组血清Smac为(288.93±98.20) ng/L,明显低于对照组(P<0.05),而PRL为(568.39±101.12) k U/L,明显高于对照组(P<0.05);观察组子宫内膜厚度为(6.12±1.14) mm,明显低于对照组(P<0.05);子宫内膜异位症患者血清Smac与子宫内膜厚度呈正相关(r=0.612,P<0.05),PRL与子宫内膜厚度呈负相关(r=-0.599,P<0.05);血清Smac与PRL呈负相关(r=-0.697,P<0.05)。结论子宫内膜异位症患者血清Smac降低,而PRL升高,其与患者子宫内膜厚度有一定相关性。
Hepatic steatosis is a frequent histological alteration in chronic hepatitis C virus (HCV) infection that sensitizes the liver to cell injury, inflammation, and fibrosis via unclear mechanisms. Although apoptosis has been implicated in various liver diseases, its importance in HCV-associated steatosis is largely unknown. In this study, we investigated the role of caspases, the key regulators of apoptosis, and employed two novel caspase assays, an immunological and a luminometric enzyme test, to detect hepatic caspase activation in sera from HCV patients with different grades of steatosis. Our data show that increased caspase activation can be found not only in liver biopsies, but also in sera from HCV patients with liver steatosis. Patients with steatosis exhibited significantly higher serum levels of caspase activity compared with normal healthy individuals. Moreover, the extent of steatosis closely correlated with serum caspase activity, whereas in particular in cases of low or moderate steatosis, no correlation was found with aminotransferase levels. In conclusion, apoptotic caspase activation is considerably elevated in HCV-associated steatosis. More importantly, our data imply that measurement of caspase activation might be a sensitive serum biomarker to detect liver steatosis in patients with chronic HCV infection and other liver diseases.