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姜黄素活性化合物——姜黄素通过调节氧化应激和炎症对 - 诱导的肺损伤的保护作用。

Protective Effects of Thymoquinone, an Active Compound of , on Rats with -Induced Lung Injury through Regulation of Oxidative Stress and Inflammation.

机构信息

Department of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 51452, Saudi Arabia.

Department of Basic Health Sciences, College of Applied Medical Sciences, Qassim University, Buraydah 51452, Saudi Arabia.

出版信息

Molecules. 2021 May 27;26(11):3218. doi: 10.3390/molecules26113218.

Abstract

Benzopyrene [B(a)P] is a well-recognized environmental carcinogen, which promotes oxidative stress, inflammation, and other metabolic complications. In the current study, the therapeutic effects of thymoquinone (TQ) against B(a)P-induced lung injury in experimental rats were examined. B(a)P used at 50 mg/kg b.w. induced lung injury that was investigated via the evaluation of lipid profile, inflammatory markers, nitric oxide (NO), and malondialdehyde (MDA) levels. B(a)P also led to a decrease in superoxide dismutase (SOD) (34.3 vs. 58.5 U/mg protein), glutathione peroxidase (GPx) (42.4 vs. 72.8 U/mg protein), catalase (CAT) (21.2 vs. 30.5 U/mg protein), and total antioxidant capacity compared to normal animals. Treatment with TQ, used at 50 mg/kg b.w., led to a significant reduction in triglycerides (TG) (196.2 vs. 233.7 mg/dL), total cholesterol (TC) (107.2 vs. 129.3 mg/dL), and inflammatory markers and increased the antioxidant enzyme level in comparison with the group that was administered B(a)P only ( < 0.05). B(a)P administration led to the thickening of lung epithelium, increased inflammatory cell infiltration, damaged lung tissue architecture, and led to accumulation of collagen fibres as studied through haematoxylin and eosin (H&E), Sirius red, and Masson's trichrome staining. Moreover, the recognition of apoptotic nuclei and expression pattern of NF-κB were evaluated through the TUNEL assay and immunohistochemistry, respectively. The histopathological changes were found to be considerably low in the TQ-treated animal group. The TUNEL-positive cells increased significantly in the B(a)P-induced group, whereas the TQ-treated group showed a decreased apoptosis rate. Significantly high cytoplasmic expression of NF-κB in the B(a)P-induced group was seen, and this expression was prominently reduced in the TQ-treated group. Our results suggest that TQ can be used in the protection against benzopyrene-caused lung injury.

摘要

苯并[a]芘[B(a)P]是一种公认的环境致癌物,可促进氧化应激、炎症和其他代谢并发症。在本研究中,研究了百里醌(TQ)对实验大鼠 B(a)P 诱导的肺损伤的治疗作用。B(a)P 以 50mg/kg b.w. 诱导肺损伤,通过评估脂质谱、炎症标志物、一氧化氮(NO)和丙二醛(MDA)水平进行研究。B(a)P 还导致超氧化物歧化酶(SOD)(34.3 vs. 58.5 U/mg 蛋白)、谷胱甘肽过氧化物酶(GPx)(42.4 vs. 72.8 U/mg 蛋白)、过氧化氢酶(CAT)(21.2 vs. 30.5 U/mg 蛋白)和总抗氧化能力比正常动物降低。用 50mg/kg b.w. 的 TQ 治疗可显著降低甘油三酯(TG)(196.2 vs. 233.7mg/dL)、总胆固醇(TC)(107.2 vs. 129.3mg/dL)和炎症标志物,并与仅给予 B(a)P 的组相比增加抗氧化酶水平(<0.05)。B(a)P 给药导致肺上皮增厚、炎症细胞浸润增加、肺组织结构受损,并导致胶原蛋白纤维积累,如通过苏木精和伊红(H&E)、天狼猩红和 Masson 三色染色研究。此外,通过 TUNEL 测定和免疫组织化学分别评估了凋亡核的识别和 NF-κB 的表达模式。在 TQ 治疗的动物组中,发现组织病理学变化明显较低。B(a)P 诱导组的 TUNEL 阳性细胞显著增加,而 TQ 治疗组的凋亡率降低。B(a)P 诱导组细胞质中 NF-κB 的表达明显升高,而 TQ 治疗组的表达明显降低。我们的结果表明,TQ 可用于保护苯并[a]芘引起的肺损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ed7/8199466/2cb7fc788688/molecules-26-03218-g001.jpg

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