Shoeib Heba Mamdoh, Keshk Walaa Arafa, Foda Abdallah Mahmoud, Abo El Noeman Saad El-Deen Abd Elfatah
Department of Medical Biochemistry & Molecular Biology, Faculty of Medicine, Tanta University, Tanta, Egypt.
Can J Physiol Pharmacol. 2018 Jun;96(6):630-636. doi: 10.1139/cjpp-2017-0738. Epub 2018 Feb 14.
Hepatic fibrosis is a worldwide health problem with significant morbidity and mortality. Currently, there is no effective therapy for hepatic fibrosis. The present study was aimed to evaluate the possible regenerative effect of platelet-rich plasma (PRP) against thioacetamide (TAA)-induced hepatic damage. Eighty albino rats were included; 40 were used for PRP preparation and 40 were randomly divided into 4 groups: group I (control group); group II (PRP control); group III (TAA-intoxicated by a dose of 200 mg/kg body mass, intraperitoneally, twice weekly for 7 weeks), and group IV (TAA intoxicated + PRP treated). Macrophage inflammatory protein-1α (MIP-1α) and cyclic adenosine monophosphate (cAMP) were immunoassayed in addition to peroxinitrite level, NADPH-quinone oxidoreductase-1 (NQO1) enzyme activity, and liver function. PRP treatment showed significant improvement in hepatic function, and decreased MIP-1α and peroxinitrite levels. Meanwhile, significant increase in NQO1 enzyme activity and cAMP level were observed. The histopathological results confirmed the laboratory results with improvement of hepatic architecture except for some inflammatory cellular infiltrates. This study shows that PRP has the ability to protect against TAA-induced liver damage, possibly by improving redox status, liver histopathological architecture, and disruption of the inflammatory and fibrotic response induced by TAA.
肝纤维化是一个全球性的健康问题，具有较高的发病率和死亡率。目前，尚无有效的肝纤维化治疗方法。本研究旨在评估富血小板血浆（PRP）对硫代乙酰胺（TAA）诱导的肝损伤可能的再生作用。纳入80只白化大鼠；40只用于制备PRP，另外40只随机分为4组：第一组（对照组）；第二组（PRP对照组）；第三组（以200mg/kg体重的剂量腹腔注射TAA，每周两次，共7周），以及第四组（TAA中毒+PRP治疗组）。除了检测过氧亚硝酸盐水平、NADPH-醌氧化还原酶-1（NQO1）酶活性和肝功能外，还对巨噬细胞炎性蛋白-1α（MIP-1α）和环磷酸腺苷（cAMP）进行了免疫测定。PRP治疗显示肝功能有显著改善，MIP-1α和过氧亚硝酸盐水平降低。同时，观察到NQO1酶活性和cAMP水平显著升高。组织病理学结果证实了实验室结果，肝脏结构有所改善，但仍有一些炎性细胞浸润。本研究表明，PRP具有预防TAA诱导的肝损伤的能力，可能是通过改善氧化还原状态、肝脏组织病理学结构以及破坏TAA诱导的炎症和纤维化反应来实现的。
