Effect of Bushen Tongluo Prescription on TGF-β1/Smads Pathway in Pulmonary Fibrosis Rats / 中国实验方剂学杂志

Objective:To observe the effect of Bushen Tongluo prescription on the pathogenesis of lung fibrosis induced by bleomycin and the transforming growth factor β1(TGF-β1)/Smads pathway protein in rats,and reveal the mechanism of this formula in inhibiting pulmonary fibrosis. Method:Totally 48 male SD rats were randomly divided into five groups:normal group(8 rats),model group(10 rats),high and low-dose Bushen Tongluo group(10 rats)and hydrocortisone sodium succinate group(10 rats). The model of pulmonary fibrosis was made with bleomycin except for normal group.Since day 3 after surgery,14.2,7.1 g·kg-1 Bushen Tongluo prescription were given by ig in high and low-dose Bushen Tongluo groups,and 4.58 g·kg-1 hydrocortisone sodium succinate was given by gavage(ig) in normal group and model group.All of the rats were put to death after 28 days.The contents of hydroxyproline (HYP),hyaluronic acid (HA) and laminin (LN) were measured after the death of the rats.Hematoxylin-eosin staining (HE) and Masson tricolor staining were used to observe the pathological changes of lung tissue. Real-time PCR and Western blot were used to observe the changes of mRNA and protein expressions of lung tissues TGF-β1, Smad2, Smad3, Smad7 in each group. Result:Compared with normal group, the level of pulmonary fibrosis was more significant in model group, and the serum HYP,HA and LN were increased obviously(PPβ1, Smad2,Smad3 proteins and mRNA in lung tissues were increased obviously(PPPPPβ1, Smad2, Smad3 protein and mRNA were decreased obviously(PPConclusion:Bushen Tongluo prescription can effectively improve the pathological process of pulmonary fibrosis, and the mechanism may be related to the regulation of TGF-β1/Smads pathway.

Effect of Zhongfengkang on the content of insulin-like growth factor-1 in brain of the rats with focal cerebral ischemia / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the effect of Zhongfengkang on the content of insulin-like growth factor-1 (IGF-1) in brain of focal cerebral ischemia rats.</p><p><b>METHOD</b>The model of focal cerebral ischemia was made by thread-blocking method. In comparison with the curative effect of buchangnaoxintong, the action of Zhongfengkang on infarct volume and the content of IGF-1 in brain of focal cerebral ischemia rats were observed in 6, 12, 24 h and 48 h after cerebral ischemia.</p><p><b>RESULT</b>As compared with sham operation group, the content of IGF-1 in brain of model group was gradually increased from 6th hour after cerebral ischemia, reaching to the maximal level at 24th hour after the onset of cerebral ischemia (P < 0.01). In comparison with the values in model group at the corresponding time points, the content of IGF-1 in brain of each treatment groups was increased in different extent with a maximal enhancement in the group treated by the high dose of Zhongfengkang (P < 0. 05 or P < 0.01); while the infarct volume of each treatment groups were decreased significantly (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Zhongfengkang could effectively protect the cerebral tissue from injury of focal cerebral ischemia in the rats through increasing the cerebral content of IGF-1 and reducing infarct volume.</p>

Effect of zhitiaokang capsule on serum insulin-like growth factor-2 in patients with hyperlipidemia / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the effect of Zhitiaokang capsule (ZTK) on serum insulin-like growth factor-2 (IGF-2) in patients with hyperlipidemia (HLP).</p><p><b>METHODS</b>Patients with HLP were randomly divided into the treated group (n = 124) and the control group (n = 62), they were treated by ZTK and Zhibituo tablet respectively for 8 weeks as one therapeutic course. The changes of blood lipids and serum IGF-2 before and after treatment were observed.</p><p><b>RESULTS</b>ZTK could significantly reduce blood lipids and increase serum content of IGF-2.</p><p><b>CONCLUSION</b>ZTK could improve the insulin resistant status and inhibit the development of hyperlipidemia in patients by means of raising serum content of IGF-2 and suppressing vascular endothelial cell apoptosis.</p>