ABSTRACT

The aim of this study was to investigate histopathological and inflammatory response in liver and kidney of rats after crack exposure. For this purpose, a total of 32 male Wistar rats were distributed into four groups: (G1) and (G2): received 18 mg/kg of body weight (b.w) of crack cocaine, but Group G2 remained 72 h without exposure after the experimental period (5 days). Experimental group 3 (G3): received 36 mg/kg of body weight (b.w) of crack cocaine. Control Group (CTRL): received only the vehicle (DMSO) administered by intraperitoneal (i.p) route for 5 days. The results showed that crack cocaine induced histopathological changes in liver and kidney. Immunohistochemistry data revealed that G2 group showed a higher immunoexpression of Ki-67 in hepatic and renal tissues. Regarding inflammation, the results showed that all groups exposed to crack cocaine decreased the expression of TNF-α, IL-6, and IL-10 in liver and kidney. In summary, our results showed that the subacute doses of crack cocaine used in this study had cytotoxic, and immunosuppressive effects in liver and kidney of rats, especially at 36 mg/kg dose. Since cellular death and inflammation participates in the multi-step process of chemical carcinogenesis, these data offer new insights into potential ways to understand the pathobiological mechanisms induced by crack cocaine in several tissues and organs.

摘要

本研究的目的是研究裂纹暴露后大鼠肝脏和肾脏的组织病理学和炎症反应。为此，将总共 32 只雄性 Wistar 大鼠分为四组：（G1）和（G2）：接受 18 mg/kg 体重（bw）的可卡因，但 G2 组在实验期（5天）。实验组 3 (G3)：接受 36 mg/kg 体重 (bw) 的可卡因。对照组（CTRL）：仅接受通过腹膜内（ip）途径施用的载体（DMSO）5天。结果表明，可卡因可引起肝脏和肾脏的组织病理学变化。免疫组化数据显示G2组肝肾组织中Ki-67的免疫表达较高。关于炎症，结果显示，所有可卡因暴露组均降低了肝脏和肾脏中TNF-α、IL-6和IL-10的表达。总之，我们的研究结果表明，本研究中使用的亚急性剂量的快克可卡因对大鼠的肝脏和肾脏具有细胞毒性和免疫抑制作用，尤其是在 36 mg/kg 剂量下。由于细胞死亡和炎症参与了化学致癌的多步骤过程，这些数据为了解可卡因在几种组织和器官中诱导的病理生物学机制的潜在方法提供了新的见解。