Physiology-Pharmacology Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Department of Physiology and Pharmacology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Mol Biol Rep. 2022 Mar;49(3):1763-1771. doi: 10.1007/s11033-021-06985-8. Epub 2022 Jan 12.
Acetaminophen overdose causes renal injury via oxidative stress and apoptosis induction. Carvacrol has several pharmacological properties such as antioxidant, anti-inflammation and anti-apoptotic effect. The aim of this study was to determine the protective effect of carvacrol on acetaminophen-induced renal damage in rats.
Forty male Wistar rats were randomly divided to five groups (n = 8) including control, carvacrol 10 mg/kg, acetaminophen, acetaminophen + carvacrol 5 mg/kg, and acetaminophen + carvacrol 10 mg/kg. Animals received a single dose of acetaminophen (500 mg/kg), then were treated with carvacrol for 1 week (daily). Afterwards, renal blood flow (RBF), mean arterial pressure, renal perfusion pressure, renal vascular resistance (RVR), blood urea nitrogen (BUN), and serum creatinine were measured. Also, malondialdehyde (MDA) concentration, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity levels were measured in the kidney tissue. Hematoxylin and eosin method was used for histological assessment. The Western blotting analysis was used to determine the Bax, Bcl-2 and cleaved caspase-3 proteins expression level in the kidney tissue. Carvacrol (10 mg/kg) significantly increased the RBF, GPx and SOD activities and also reduced the RVR, serum creatinine, BUN, and MDA in the acetaminophen + carvacrol 10 mg/kg group versus acetaminophen group (P < 0.05). Also, carvacrol significantly decreased the cleaved caspase-3, Bax proteins expression level, and kidney tissue damage score in the acetaminophen + carvacrol 10 mg/kg group versus acetaminophen group (P < 0.05).
This study showed that carvacrol can attenuate the acetaminophen induced acute kidney damage via suppressing oxidative stress and apoptosis biochemical factors.
对乙酰氨基酚过量会通过氧化应激和诱导细胞凋亡导致肾损伤。香芹酚具有抗氧化、抗炎和抗凋亡作用等多种药理特性。本研究旨在确定香芹酚对大鼠乙酰氨基酚诱导的肾损伤的保护作用。
40 只雄性 Wistar 大鼠随机分为五组（n=8），包括对照组、香芹酚 10mg/kg 组、乙酰氨基酚组、乙酰氨基酚+香芹酚 5mg/kg 组和乙酰氨基酚+香芹酚 10mg/kg 组。动物给予单次剂量的乙酰氨基酚（500mg/kg），然后用香芹酚治疗 1 周（每日）。之后，测量肾血流量（RBF）、平均动脉压、肾灌注压、肾血管阻力（RVR）、血尿素氮（BUN）和血清肌酐。同时，测量肾组织中的丙二醛（MDA）浓度、谷胱甘肽过氧化物酶（GPx）和超氧化物歧化酶（SOD）活性水平。采用苏木精和伊红法进行组织学评估。采用 Western blotting 分析测定肾组织中 Bax、Bcl-2 和 cleaved caspase-3 蛋白的表达水平。香芹酚（10mg/kg）可显著增加 RBF、GPx 和 SOD 活性，并降低乙酰氨基酚+香芹酚 10mg/kg 组与乙酰氨基酚组的 RVR、血清肌酐、BUN 和 MDA（P<0.05）。此外，香芹酚可显著降低乙酰氨基酚+香芹酚 10mg/kg 组与乙酰氨基酚组的 cleaved caspase-3 和 Bax 蛋白表达水平和肾组织损伤评分（P<0.05）。
本研究表明，香芹酚通过抑制氧化应激和凋亡生化因子，可减轻乙酰氨基酚引起的急性肾损伤。
