The cardiovascular protective effect and mechanism of calycosin and its derivatives / 中国天然药物

Cardiovascular disease is the main cause of mortality and morbidity in the world, especially in developing countries. Drug therapy is one of the main ways to treat cardiovascular diseases. Among them, great progress has been made in the treatment of cardiovascular diseases with traditional Chinese medicine. In terms of experimental research, the mechanism of traditional Chinese medicine in the treatment of cardiovascular diseases has been thoroughly discussed in vitro and in vivo. In terms of clinical treatment, traditional Chinese medicine with flavonoids, saponins and alkaloids as the main effective components has a definite effect on the treatment of cardiovascular diseases such as arrhythmia, myocardial ischemia, angina pectoris and myocardial infarction, with high safety and good application prospects. With the further research on the effective ingredients, mechanism and adverse reactions of traditional Chinese medicine, it will be beneficial to the effectiveness of traditional Chinese medicine, reduce side effects and promote the modernization of traditional Chinese medicine. Calycosin and its derivatives, the main bioactive flavonoids in Astragalus membranaceus have multiple biological effects, such as antioxidant, pro-angiogenesis, anti-tumour, and anti-inflammatory effects. Based on the above biological effects, calycosin has been shown to have good potential for cardiovascular protection. The potent antioxidant effect of calycosin may play an important role in the cardiovascular protective potential. For injured cardiac myocytes, calycosin and its derivatives can alleviate the cell damage mainly marked by the release of myocardial enzymes and reduce the death level of cardiac myocytes mainly characterized by apoptosis through various mechanisms. For vascular endothelial cells, calycosin also has multiple effects and multiple mechanisms, such as promoting vascular endothelial cell proliferation, exerting vasodilating effect and directly affecting the synthesis function of endothelial cells. The present review will address the bioactivity of calycosin in cardiovascular diseases such as protective effects on cardiac myocytes and vascular endothelial cells and elucidate main mechanism of calycosin and its derivatives to exert the above biological effects.

Effect of angelicanaphtha on proliferation, apoptosis, collagen synthesis of human umbilical vein endothelial cells / 中华整形外科杂志

<p><b>OBJECTIVE</b>To investigate the effects of angelicanaphtha on proliferation, cell cycle, apoptosis, and collagen synthesis of human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>HUVEC was cultured and passaged in Dulbecco's modified Eagle's medium (DMEM) and treated with angelicanaphtha 1 mg/ L, 4 mg/L, and 16 mg/L at 1, 3, 5, and 7 day respectively. The proliferation was measured with MTT method. The cell cycle and apoptosis were analyzed with flow cytometry and collagen synthesis was determined with radioimmunoassay.</p><p><b>RESULTS</b>The proliferation of the HUVEC was accelerated by angelicanaphtha < or =4 mg/L and inhibited by angelicanaphtha at 16 mg/L (P < 0.05). Lower concentration (< or = 4 mg/L) of Angelicanaphtha decreased cells in G0/G1 phase and increased significantly cells in S phase and inhibited the apoptosis (P < 0.05). However, angelicanaphtha at 16 mg/L increased cells in G0/G1 phase and decreased cells in S phase and induced the apoptosis (P < 0.05). The collagen synthesis of HUVEC was inhibited by angelicanaphtha in concentration-dependent manner (P < 0.05 or 0.01).</p><p><b>CONCLUSION</b>The proliferation effects of angelicanaphtha on HUVEC had dualistic regulation of increase by lower-concentration and inhibition by higher-concentration. Collagen synthesis of HUVEC was inhibited by angelicanaphtha in concentration-dependent manner.</p>

Activity changes of protein kinase C in effect of interferon-gamma on wound healing and cicatrisation / 中华整形外科杂志

<p><b>OBJECTIVE</b>To study the roles of protein kinase C (PKC) in effect of interferon-gamma (IFN-gamma) on wound healing and cicatrization.</p><p><b>METHODS</b>IFN-gamma was applied on the wound and into the scar tissues of rabbit ear before or after wound healing. PKC activities in the tissues from 0, 3, 6 d, 11-16 d post-wounding and from 14, 30 and 45d post-epithelization were measured by phosphorus (32p) incorporation. The time of wound epithelization and scar changes were also observed.</p><p><b>RESULTS</b>The PKC activity in granulation tissue, wound margin tissue and scar tissue elevated obviously in comparing with that of normal skin (P < 0.01). IFN-gamma did not change PKC activity (P > 0.05). But it delayed the wound healing (P < 0.01) and inhibited scar hyperplasia (P <0.05).</p><p><b>CONCLUSIONS</b>PKC might not mediate the signal of IFN-gamma inhibiting the wound healing and scar hyperplasia. But PKC might be related to the wound healing and scar hyperplasia.</p>

Signal roles of protein tyrosine kinase in transforming growth factor-beta1, or interferon-gamma regulated proliferation and collagen synthesis by fibroblasts from hypertrophic scar and normal dermis / 中华整形外科杂志

<p><b>OBJECTIVE</b>To study the signal roles of protein tyrosine kinase (PTK) on proliferation and collagen synthesis of fibroblasts derived from hypertrophic scar(HS-FB) and normal skin (NS-FB) by interferon-gamma (IFN-gamma) or transforming growth factor beta1 (TGF-beta1).</p><p><b>METHODS</b>HS-FB and NS-FB were cultured and passaged in Dulbecco's modified Eagle's medium(DMEM). The PTK activity in unstimulated or IFN-gamma or TGF-beta1-stimulated HS-FB and NS-FB (10,30,60 and 120 min) were assayed by phosphorus (32P) incorporation. Cell proliferation was determined with MTT stain. The type III procollagen was measured by radioimmunoassay.</p><p><b>RESULTS</b>TGF-beta1 did not change PTK activity but it increased predominately proliferation and collagen synthesis of HS-FB and NS-FB in time-dependent fashion. Genistein, an inhibitor of PTK, inhibited HS-FB and NS-FB to proliferate and synthesize collagen but it could not change the roles on proliferation and collagen synthesis by TGF-beta1. IFN-gamma activated transiently PTK (P < 0.05) and increased proliferation and collagen synthesis of both fibroblast (P < 0.05, at 30 min, 60 min). As the recovery of PTK activity, the proliferation and collagen synthesis were inhibited by IFN-gamma at 120 min. Furthermore, Genistein abrogated the transient increased roles and partly reversed the longterm inhibitory functions by IFN-gamma (P < 0.05) . There were no difference on PTK activity, proliferation and collagen synthesis between HS-FB and NS-FB.</p><p><b>CONCLUSIONS</b>PTK did not mediate the signal of TGF-beta1 but transduced the signal of transient increased roles of IFN-gamma. Inhibited or activated PTK might mediate the signal of decreasing or increasing proliferation and collagen synthesis of fibroblast.</p>