Thymoquinone effectively alleviates lung fibrosis induced by paraquat herbicide through down-regulation of pro-fibrotic genes and inhibition of oxidative stress

被引:51
作者
Pourgholamhossein, Fatemeh [1 ,2 ]
Sharififar, Fariba [3 ]
Rasooli, Rokhsana [1 ,2 ]
Pourgholi, Leyla [2 ]
Nakhaeipour, Fatemeh [2 ]
Samareh-Fekri, Hojjat [4 ]
Iranpour, Maryam [6 ]
Mandegary, Ali [2 ,5 ]
机构
[1] Kerman Univ Med Sci, Neuropharmacol Inst, Pharmaceut Res Ctr, Haft Bagh Blvd, Kerman 7616911319, Iran
[2] Kerman Univ Med Sci, Sch Pharm, Dept Pharmacol & Toxicol, Haft Bagh Blvd, Kerman 7616911319, Iran
[3] Sch Pharm, Dept Pharmacognosy Herbal & Tradit Med, Res Ctr, Haft Bagh Blvd, Kerman 7616911319, Iran
[4] Kerman Univ Med Sci, Deputy Res, Cent Res Lab, Haft Bagh Blvd, Kerman 7616911319, Iran
[5] Kerman Univ Med Sci, Afzalipours Hosp, Inst Basic & Clin Physiol Sci, Gastroenterol & Hepatol Res Ctr, Imam Highway, Kerman 7616913911, Iran
[6] Kerman Univ Med Sci, Pathol & Stem Cell Res Ctr, Kerman 7617939555, Iran
关键词
Thymoquinone; Pulmonary fibrosis; Paraquat; Oxidative stress; Gene expression; INDUCED PULMONARY-FIBROSIS; TGF-BETA; EXPRESSION; RATS; MICE; MECHANISMS; TOXICITY; INJURY;
D O I
10.1016/j.etap.2016.06.019
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The potential preventive and therapeutic effects of thymoquinone (TQ) and its molecular mechanism were evaluated in paraquat (PQ)-induced pulmonary fibrosis in mice. TQ was administered orally at the doses of 20 and 40 mg/kg during the course and after development of fibrosis. Pathological changes, expressions of genes involved in fibrogenesis, hydroxyproline (HP) and oxidative stress parameters were determined in the lung tissues. TQ dose-dependently recovered the pathological changes induced by PQ TQ decreased hydroxyproline content, lipid peroxidation and restored the antioxidant enzymes to the normal values. In molecular level, expressions of TGF-beta 1, alpha-SMA, collagen 1a1 and collagen 4a1 genes were also returned to the control level by TQ, This study indicated that TQ has the preventive and therapeutic potentials for the treatment of lung fibrosis by inhibition of oxidative stress and down regulation of profibrotic genes. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:340 / 345
页数:6
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