Shafaroodi Hamed, Hashemi Mehrdad, Sharif Zahra Nadia, Moezi Leila, Janahmadi Zeinab, Dehpour Ahmad Reza
Department of Pharmacology and Toxicology, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran.
Department of Molecular Genetics, Tehran Medical Branch, Islamic Azad University, Tehran, Iran.
Acta Med Iran. 2017 Jan;55(1):29-34.
Cirrhosis has been related with hyperdynamic circulation, manifesting as increased cardiac output and decreased systemic vascular resistance. In the present study we examined the cirrhosis outcome on apoptosis of rat hearts. We also tried to explore the role of nitric oxide (NO) and oxidative stress in the probable changed apoptosis of cirrhotic hearts. Twenty eight days after ligation of bile duct, heart tissues were tested for apoptosis. The extent of malondialdehyde (MDA), and the activities of catalase (CAT), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD) have been calculated in heart tissues. The cirrhotic hearts exhibited structural defects and greater apoptosis. Chronic treatment of cirrhotic rats with L-NAME, a non-selective inhibitor of NO synthase, inhibited heart structural defects and reduced apoptosis of hearts. We also showed that cirrhotic rat hearts had an enhanced level of MDA and reduced activities of CAT, GSHPx and SOD. When the animals were treated by L-NAME chronically, the MDA level reduced and activities of CAT, GSHPx and SOD augmented in cirrhotic heart. In conclusion, increased apoptosis of cirrhotic hearts probably happen due to NO overproduction and increased oxidative stress in hearts of cirrhotic rats.
肝硬化与高动力循环有关，表现为心输出量增加和全身血管阻力降低。在本研究中，我们检测了肝硬化对大鼠心脏细胞凋亡的影响。我们还试图探讨一氧化氮（NO）和氧化应激在肝硬化心脏可能发生的细胞凋亡变化中的作用。胆管结扎28天后，检测心脏组织的细胞凋亡情况。计算心脏组织中丙二醛（MDA）的含量以及过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSHPx）和超氧化物歧化酶（SOD）的活性。肝硬化心脏表现出结构缺陷和更多的细胞凋亡。用L-NAME（一种非选择性一氧化氮合酶抑制剂）对肝硬化大鼠进行长期治疗，可抑制心脏结构缺陷并减少心脏细胞凋亡。我们还发现，肝硬化大鼠心脏的MDA水平升高，CAT、GSHPx和SOD的活性降低。当动物长期接受L-NAME治疗时，肝硬化心脏的MDA水平降低，CAT、GSHPx和SOD的活性增强。总之，肝硬化心脏细胞凋亡增加可能是由于肝硬化大鼠心脏中NO产生过多和氧化应激增加所致。
