Department of Pharmacology, Faculty of Pharmacy, Ataturk University, 25240 Erzurum, Turkey.
Naunyn Schmiedebergs Arch Pharmacol. 2010 May;381(5):455-66. doi: 10.1007/s00210-010-0504-y. Epub 2010 Mar 27.
The aim of this study was to evaluate the effects of atorvastatin as an antioxidant and tissue protective agent and study the biochemical and histopathological changes in experimental ischemia and ischemia/reperfusion (I/R) injury in rat ovaries. The experiment used 48 adult female rats, and the experimental groups can be summarized as: group I, a sham operation; group II, a sham operation +10 mg/kg atorvastatin; group III, bilateral ovarian ischemia; and groups IV and V, bilateral ovarian ischemia +5 and 10 mg/kg atorvastatin before 30 min of ischemia, respectively (after a 3-h period of ischemia, the bilateral ovaries were surgically removed); group VI, 3-h period of ischemia followed by 3-h reperfusion; groups VII and VIII received 5 and 10 mg/kg atorvastatin, respectively, 2.5 h after the induction of ischemia, and at the end of a 3-h period of ischemia, bilateral vascular clips were removed and 3-h reperfusion continued. After the experiments, superoxide dismutase (SOD) and myeloperoxidase (MPO) activity and levels of glutathione (GSH) and lipid peroxidation (LPO) were determined, and histopathological changes were examined in all rat ovarian tissue. Ischemia and I/R increased the LPO level and MPO activity while decreasing the SOD activity and GSH level significantly in comparison to the sham group. The 5- and 10-mg/kg doses of atorvastatin before ischemia and I/R reversed the trend in LPO level and MPO activity. The levels of SOD and GSH were decreased by ischemia and I/R. The administration of atorvastatin before ischemia and I/R treatments also reversed the trend in the SOD and GSH levels. In the I/R plus atorvastatin groups, although minimal vascular dilation in the ovary stoma and some degenerative cell clusters were seen, most of the cellular structures showed no pathological changes. Administration of atorvastatin is effective in reversing tissue damage induced by ischemia and/or I/R in ovaries.
本研究旨在评估阿托伐他汀作为抗氧化剂和组织保护剂的作用,并研究大鼠卵巢缺血和缺血/再灌注(I/R)损伤的生化和组织病理学变化。实验采用 48 只成年雌性大鼠,实验分组可概括为:I 组,假手术;II 组,假手术+10mg/kg 阿托伐他汀;III 组,双侧卵巢缺血;IV 组和 V 组,分别在缺血前 30 分钟给予 5 和 10mg/kg 阿托伐他汀;VI 组,缺血 3 小时后再灌注 3 小时;VII 组和 VIII 组分别在诱导缺血后 2.5 小时给予 5 和 10mg/kg 阿托伐他汀,在缺血 3 小时结束时,去除双侧血管夹并继续再灌注 3 小时。实验结束后,测定大鼠卵巢组织中超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性及谷胱甘肽(GSH)和脂质过氧化(LPO)水平,并观察所有大鼠卵巢组织的组织病理学变化。与假手术组相比,缺血和 I/R 导致 LPO 水平和 MPO 活性显著升高,而 SOD 活性和 GSH 水平显著降低。缺血和 I/R 前给予 5 和 10mg/kg 阿托伐他汀逆转了 LPO 水平和 MPO 活性的趋势。SOD 和 GSH 水平在缺血和 I/R 后降低。缺血和 I/R 前给予阿托伐他汀也逆转了 SOD 和 GSH 水平的趋势。在 I/R 加阿托伐他汀组中,尽管卵巢门处的血管扩张轻微,一些退行性细胞簇可见,但大多数细胞结构无明显病理改变。阿托伐他汀的给药可有效逆转卵巢缺血和/或 I/R 引起的组织损伤。