Chiorescu Stefan, Andercou Octavian Aurel, Grad Nicolae Ovidiu, Mironiuc Ion Aurel
2nd Surgery Department, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Clujul Med. 2018;91(1):79-84. doi: 10.15386/cjmed-859. Epub 2018 Jan 15.
The purpose of this experimental study was to demonstrate the reduction of peritoneal adhesions formation in rats after intraperitoneal administration of rosuvastatin, due to its anti-inflammatory effect.
Peritoneal adhesions were induced in 120 Wistar-Bratislava rats divided into 4 groups (n=30), using a parietal and visceral (cecal) abrasion model. Group I was designated as control group; in group II, a saline solution was administered intraperitoneally; in groups III and IV, a single dose of rosuvastatin solution, 10 mg/kg and 5 mg/kg respectively, was injected intraperitoneally. The serum values of tumor necrosis factor (TNF-α) and interleukin-1 (IL-1α) were determined on day 1 and day 7 postoperatively (ELISA). Macroscopic assessment of the peritoneal adhesions was conducted on day 14.
Rosuvastatin therapy induced a significant decrease of tumor necrosis factor serum levels in groups III and IV, on day 1 and day 7 (p<0.01). Intraperitoneal administration of rosuvastatin correlated with a decrease of mean interleukin-1α levels on postoperative day 1 in groups III (p=0.0013) and IV (p=0.00011), but not on day 7, where the differences were no longer statistically significant (p=0.8) The reduction of postoperative peritoneal adhesions in the experimental rat model is supported by the anti-inflammatory effect of rosuvastatin, mediated mainly by the tumor necrosis factor.
Rosuvastatin prevents the formation of postoperative peritoneal adhesions in rats. This effect may be linked to the inhibition of proinflammatory cytokines release in the early stages of adhesions formation. The present study suggests that rosuvastatin may be an efficient pharmacological agent in the prevention of postoperative peritoneal adhesions development, and requires further studies as it has a promising application value.
本实验研究的目的是证明腹腔注射瑞舒伐他汀后，因其抗炎作用可减少大鼠腹膜粘连的形成。
采用壁层和脏层（盲肠）擦伤模型，将120只Wistar - 布拉迪斯拉发大鼠分为4组（每组n = 30只），诱导形成腹膜粘连。第一组为对照组；第二组腹腔注射生理盐水；第三组和第四组分别腹腔注射单剂量10mg/kg和5mg/kg的瑞舒伐他汀溶液。术后第1天和第7天测定肿瘤坏死因子（TNF-α）和白细胞介素-1（IL-1α）的血清值（酶联免疫吸附测定法）。术后第14天对腹膜粘连进行宏观评估。
在第1天和第7天，瑞舒伐他汀治疗使第三组和第四组的肿瘤坏死因子血清水平显著降低（p<0.01）。腹腔注射瑞舒伐他汀与第三组（p = 0.0013）和第四组（p = 0.00011）术后第1天平均白细胞介素-1α水平的降低相关，但在第7天差异不再具有统计学意义（p = 0.8）。瑞舒伐他汀的抗炎作用主要由肿瘤坏死因子介导，支持了实验大鼠模型中术后腹膜粘连的减少。
瑞舒伐他汀可预防大鼠术后腹膜粘连的形成。这种作用可能与粘连形成早期促炎细胞因子释放的抑制有关。本研究表明，瑞舒伐他汀可能是预防术后腹膜粘连发展的一种有效药物，因其具有广阔的应用前景，需要进一步研究。
