RESUMO
Objective To investigate the relationship between gene polymorphisms of homocysteine (Hcy), metabolic enzymes methylenetetrahydrofolate reductase MTHFR C677T and chronic pulmonary heart disease (CPHD). Methods The gene polymorphisms of MTHFR C677T were determined by the polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP)in CPHD patients (n=120) and healthy control (HC, n=120), and genotyping was carried on. The automatic biochemistry analyzer was used to detect the level of Hcy and other related biochemical indicators. Results There was significant difference in Hcy level between the CPHD group and HC group (P<0.05). The mutation frequencies of CC, CT and TT were 24.17%, 43.33%and 32.50%, 35.00%, 47.50%and 17.50%in the CPHD group and HC group. The mutation frequencies of allele C/T were 45.83%and 54.17%in HC group, and 58.75%and 41.25%in control group. There was significant difference in the overall frequency distribution between the three genotypes (χ2 =8.010, P<0.05). The frequency of T allele was significantly higher in CPHD group than that in control group (χ2=8.025,P<0.05). Conclusion The increased Hcy and its metabolic enzyme MTHFR C677T may be involved in the occurrence and development of CPHD.
RESUMO
Objective To investigate the effect of dihydroartemisinin on pulmonary fibrosis and its mechanism in rats.Methods Seventy-five SD rats were randomly divided into 5 groups:the control group,the model group,the high dihydroartemisinin group,the low dihydroartemisinin group,and the prednisone group(15 rats in each group).Saline(9 g/L,0.3 mL) was injected into the rat trachea of the control group,and the rats of the rest 4 groups were injected bleomycin(3 mg/kg).The rats in the control group and the model group received saline lavage (9 g/L,3 mL),while the rats in the high dihydroartemi-sinin group and the low dihydroartemisinin group received dihydroartemisinin lavage (100,50 mg/kg),and the rats in the prednisone group received prednisone lavage each day.Five rats in each group were sacrificed and lung tissues were removed on the 8th,15th,and 29th day of lavage,and the degree of inflammation in lung tissue was observed by HE staining.The deposit of collagen in lung tissue was observed by Masson staining.The expressions of transforming growth factor β1 (TGF-β1),collagen Ⅰ and collagen Ⅲ in pneumonic tissues were detected by immunohistochemistry.Results The degree of inflammation in pneumonic tissues in the high dihydroartemisinin group,the low dihydroartemisinin group,and the prednisone group were less significantly than that in the model group(all P ＜ 0.01).The deposit of collagen in lung tissues in the model group was obviously increased than that of the control group at each time points(all P ＜0.01).The deposit of collagen in lung tissues in the high dihydroartemisinin group,the low dihydroartemisinin group and the prednisone group were lower than that in the model group(all P ＜0.01),and higher than that of the control group at each time points(all P ＜0.01).There was no significant difference between the high dihydroartemisinin group and the prednisone group (P ＞ 0.05).TGF-β1,collagen Ⅰ and collagen Ⅲ in lung tissues in the high dihydroartemisinin group and the prednisone group were lower than those in the model group(P ＜0.01),and higher than those in the control group at each time points(all P ＜ 0.01).There was no significant difference in TGF-β1,collagen Ⅰ and collagen Ⅲ in lung tissue between the high dihydroartemisinin group and the prednisone group(all P ＞0.05),except that collagen Ⅲ expression in lung tissues was lower than that of the prednisone group on the 29th day (P ＞ 0.05).Conclusions Dihydroartemisinin can lessen the extent of pulmonary fibrosis in rats and its anti-fibrosis effect is dose-dependent.The anti-fibrosis effect of dihydroartemisinin may decrease the deposit of collagens in the lung tissues by inhibiting TGF-β1 expression in the lung tissues and have an effect of antifibrosis.