Abstract：Objective To observe the mechanism of heme oxygenase-1 on Silicosis fibrosis in rats. Methods 60 Wistar rats were randomly divided as follows: the control group (A) , silicon dioxide group (group B), group B + HO-1 inhibitor zinc protoporphyrin group (Group C) and group B + HO-1 inducer cobalt protoporphyrin group (group D). Instill silica suspension by using the method of tracheal exposure to duplicate the rats model with silicosis. After manufacturing the model for 28 days, observe the lung tissue pathological structures by using the HE staining, detect the HO-1 protein content and HO-1mRNA in the lung tissues of rats by using the Western blot analysis and the Expression quantitative PCR. Results The expression of HO-1 in normal control group was significantly lower than that of other groups(P<0.05). The expression of HO-1 in C group was significantly lower than that of B group, and its expression in D group was significantly higher than that of B group(P<0.05). Detected by RT-PCR, the relative expression levels of HO-1 mRNA in four groups respectively were 1,2.25 ± 0.38,1.81 ± 0.74 and 7.75 ± 0.56. The levels of HO-1mRNA in C group were significantly lower than B group and its levels in D group were significantly higher than B group(P<0.05). Conclusion HO-1 participates in the formation process of silicosis fibrosis in rats. The extent of silicosis fibrosis in rats can be changed by the intervention of HO-1. And it can provide a new approach for the diagnosis and treatment of silicosis fibrosis
[1] Leung CC,Yu IT,Chen W. Silicosis[J]. The Lancet, 2012, 379: 2008-2018. [2] Barbagallo I,Galvano F,Frigiola A, et al. Potential therapeutic effects of natural heme oxygenase-1 inducers in cardiovascular diseases[J]. Antioxidants & redox signaling, 2013, 18: 507-521. [3] Ollinger R,Pratschke J. Role of heme oxygenase-1 in transplantation[J]. Transplant international, 2010, 23 : 1071-1081. [4] Neubauer JA,Sunderram J. Heme oxygenase-1 and chronic hypoxia[J]. Respiratory physiology & neurobiology, 2012, 184 : 178-185. [5] Santos C,Norte A,Fradinho F, et al. Silicosis - brief review and experience of a pulmonology ward[J]. Revista portuguesa de pneumologia, 2010, 16: 99-115. [6] Su ZY,Shu L,Khor TO, et al. A perspective on dietary phytochemicals and cancer chemoprevention: oxidative stress, nrf2, and epigenomics[J]. Topics in current chemistry, 2013, 329: 133-162. [7] Haines DD,Lekli I,Teissier P, et al. Role of haeme oxygenase-1 in resolution of oxidative stress-related pathologies: focus on cardiovascular, lung, neurological and kidney disorders[J]. Acta physiologica, 2012, 204: 487-501. [8] Origassa CS,Camara NO. Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury[J]. World journal of hepatology, 2013, 5: 541-549. [9] Jin C,Zhou D,Lv F. Beneficial effects of early (but not late) intervention of heme oxygenase-1 on bleomycin-induced pulmonary fibrosis in mice[J]. Respiratory physiology & neurobiology, 2011, 175: 239-246. [10] Wang QM,Du JL,Duan ZJ, et al. Inhibiting heme oxygenase-1 attenuates rat liver fibrosis by removing iron accumulation[J]. World journal of gastroenterology, 2013, 19: 2921-2934. [11] Kie JH,Kapturczak MH,Traylor A,et al. Heme oxygenase-1 deficiency promotes epithelial-mesenchymal transition and renal fibrosis[J]. Journal of the American Society of Nephrology, 2008, 19: 1681-1691. [12] Wang L,Lee JY,Kwak JH, et al. Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction[J]. American journal of physiology. Renal physiology, 2007, 294: 508-517.
2014, Vol. 21 
