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Pecan pericarp extract protects against carbon tetrachloride-induced liver injury through oxidative mechanism in rats
Toxicology Research ( IF 2.1 ) Pub Date : 2020-09-24 , DOI: 10.1093/toxres/tfaa071
Hallegue Dorsaf 1 , Moujahed Sabrine 1 , Ben Lamine Houda 2 , Ben Rhouma Khémais 1 , Sakly Mohsen 1 , Tebourbi Olfa 1
Affiliation  

Abstract
The purpose of this study was to quantify the proanthocyanidin content of pecan (Carya illinoinensis) pericarp extract (PPE) and to assess its useful impacts against carbon tetrachloride (CCl4)-induced hepatotoxicity. Rats were randomly divided into four groups: Group 1: received intraperitoneal injection of saline solution, Group 2: was injected with PPE (25 mg/kg body weight) for 10 consecutive days, Group 3: received CCl4 (0.5 ml/kg, subcutaneous injection), Group 4: was coadministred with PPE + CCl4. The CCl4 was administered every 3 days during 10 days. Results revealed the presence of a high amount of total proanthocyanidins in the PPE (81.01 ± 0.21 mg TAE.g−1DW). CCl4 injection induced significant reductions in hepatic antioxidants but increased hepatic lipid peroxidation (LPO) as well as serum injury biomarkers. However, cotreatment with PPE significantly (P < 0.05) inverted CCl4-induced increase in plasma alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase activities, respectively to 74%, 77%, 60%, and 82% compared with CCl4 group. No significant toxic effects were observed following treatment with plant extract alone. PPE cotreatment also decreased significant (P < 0.05) the hepatic malondialdehyde formation (21%) and enhanced the liver catalase activity (107%) in CCl4-intoxicated rats. The histopathological examination showed inflammatory infiltration and degenerative changes in the hepatic tissue following CCl4 injection. The hepatoprotective activity of PPE against CCl4 exposure was supported by the maintenance of structural integrity of liver histopathology. In conclusion, the current study illustrated that PPE pretreatment significantly improved all examined parameters, restored the hepatic architecture and successfully alleviates oxidative damage induced by CCl4 intoxication.


中文翻译:

山核桃果皮提取物通过氧化机制保护大鼠免受四氯化碳诱导的肝损伤

摘要
本研究的目的是量化山核桃 ( Carya illinoinensis ) 果皮提取物 (PPE)的原花青素含量,并评估其对四氯化碳 (CCl 4 ) 诱导的肝毒性的有用影响。大鼠随机分为四组:第 1 组:腹腔注射生理盐水,第 2 组:连续 10 天注射 PPE(25 毫克/公斤体重),第 3 组:接受 CCl 4(0.5 毫升/公斤,皮下注射),第4组:与PPE + CCl 4共同给药。在 10 天内每 3 天施用一次CCl 4。结果显示 PPE 中存在大量总原花青素 (81.01 ± 0.21 mg TAE.g -1 DW)。四氯化碳4注射诱导肝脏抗氧化剂的显着减少,但增加肝脏脂质过氧化 (LPO) 以及血清损伤生物标志物。然而,与 CCl相比,PPE 共同处理显着 ( P < 0.05) 使 CCl 4诱导的血浆丙氨酸氨基转移酶、天冬氨酸氨基转移酶、碱性磷酸酶和乳酸脱氢酶活性分别增加了 74%、77%、60% 和 82% 4组。单独用植物提取物处理后未观察到显着的毒性作用。PPE 协同处理还显着降低了 ( P  < 0.05) 肝脏丙二醛的形成 (21%) 并增强了 CCl 4 中的肝脏过氧化氢酶活性 (107%)- 陶醉的老鼠。组织病理学检查显示炎性浸润和肝组织以下的CCl退行性改变4喷射。PPE 对 CCl 4暴露的保肝活性得到维持肝脏组织病理学结构完整性的支持。总之,目前的研究表明,PPE 预处理显着改善了所有检查参数,恢复了肝脏结构并成功减轻了由 CCl 4中毒引起的氧化损伤。
更新日期:2020-11-04
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