Mechanism of Therapeutic Methods for Activating Blood and Removing Blood Stasis in Treatment of Cerebral Hemorrhage / 中国实验方剂学杂志

Intracerebral hemorrhage (ICH) refers to the primary non-traumatic parenchymal hemorrhage, which is one of the common cerebrovascular diseases, with a high incidence, rapid development, slow recovery and high disabling rate. After intracerebral hemorrhage, a series of pathological changes occur in the brain tissue, such as local hematoma and its space occupying effect, secondary cerebral edema, death of brain cells and destruction of blood-brain barrier, which may lead to brain injury and neurological defects, seriously affect the quality of life of patients, and even endanger the life. Therefore, it is great medical value to find effective therapeutic methods and drugs, explore the mechanisms and targets for improving neurological function, reduce sequelae and improve the quality of life of patients. According to the theory of traditional Chinese medicine (TCM), cerebral hemorrhage belongs to " abnormal flow of the blood" , which equals to blood stasis. In recent years, scholars conducted extensive research on drugs for promoting blood circulation to remove blood stasis with modern scientific methods, and made in-depth discussion for the mechanism, and found that therapies for activating blood and removing blood stasis, plays a key role in intervening a series of physiological and pathological changes after cerebral hemorrhage, with significant curative effects in removing hematoma, improving the microcirculation and reducing the mortality and morbidity. This article summarized drugs for promoting blood circulation to remove blood stasis (Notoginseng Radix et Rhizoma, Salviae Miltiorrhizae Radix et Rhizoma, Hirudo), formulas (Buyang Huanwu Tang, Didangtang, Naoxueshu oral liquid, Tongqiao Huoxuetang) and compound injections (Danhong injection) for the treatment of cerebral hemorrhage targets, and discussed the experimental research progress TCM for promoting blood circulation to remove blood stasis in treatment of cerebral hemorrhage in terms of promoting hematoma absorption, reducing brain edema and apoptosis, promoting angiogenesis, inhibiting the inflammatory response, and promoting the repair and regeneration of nerve tissue in nearly five years, and summarized the therapeutic mechanism, so as to provide scientific basis for clinical application of the therapeutic methods for activating blood and removing stasis to treat cerebral hemorrhage and the modern scientific research.

Meta-Analysis for Effect of Danhong Injection on Cardiac Function and TIMI During Perioperative PCI in Acute Myocardial Infarction / 中国实验方剂学杂志

<b>Objective::Evaluate the effects of Danhong injection for perioperative percutaneous coronary intervention (PCI) on cardiac function and thrombolysis in myocardial infarction (TIMI) in patients with acute myocardial infarction (AMI). <b>Method::Computer retrieving CNKI, Wanfang database, VIP database, PubMed, CBM, Web of Science, The Cochrane Library, gathering Danhong injection in percutaneous coronary intervention perioperative application in the treatment of acute myocardial infarction clinic trials. The Cochrane risk evaluation is adopted to improve the quality of literature evaluation, with Revman 5.3 software for Meta-analysis. <b>Result::Participants included in 12 clinic trials contains a total of 1 131 patients, including 569 patients in Danhong treatment and 562 patients in control group. The results showed that compared with conventional treatment, Danhong injection treated patients had LVEF increased obviously [mean difference (MD)=6.62, 95% confidence interval (CI) (4.91, 8.34), <italic>P</italic><0.000 01], the number of TIMI class 3 patients significantly increased[relative risk (RR)=0.22, 95%CI(0.12, 0.41), <italic>P</italic><0.000 01], and BNP levels significantly decreased [MD=151.86, 95%CI (-247.00, -56.72), <italic>P</italic>=0.002]. <b>Conclusion::Danhong injection can improve the function of acute myocardial infarction after percutaneous coronary intervention.

Effect of Qingkailing on Expression of Toll-like Receptor 4, gp91phox and Zonula Occludens-1 in Cerebrovascular Endothelial Cells Induced by Hypoxia Activating Microglias / 中国康复理论与实践

Objetive To investigate the effect of Qingkailing injection on the expression of Toll-like receptor 4 (TLR4), gp91phox and zonula occludens-1 (ZO-1) in cerebrovascular endothelial cells induced by hypoxia activation of microglias. Methods:BV2 microglia cells were divided into six groups. They were cultured in serum-free DMEM, while the Qingkailing groups of low, middle and high dosages were cultured with 0.0625%, 0.125% and 0.25% Qingkailing injection, respectively, and minocycline group with minocycline of 200 nmol/L. The groups other than control group underwent hypoxia for 24 hours and reoxygenation for 24 hours. Then, the medium of microglia was put into the medium of Balb/c endothelial cells for 24 hours. The cell viability of endothelial cells was measured with CCK-8, the concentration of nitric oxide (NO) was detected with colorimetry, and the experission of TLR4, gp91phox and ZO-1 was detected with Western blotting. Results:Compared with the control group, the cell viability and the expression of ZO-1 decreased in the model group (P < 0.01), while the concentration of NO and the expression of TLR4 and gp91phox increased (P < 0.05). Compared with the model group, the cell viability and the expression of ZO-1 increased in the Qingkailing groups and the minocycline group (P < 0.05), while the concentration of NO and the expression of TLR4 and gp91phox decreased (P < 0.05). Conclusion:Qingkailing injection may enhance the survival and function of cerebrovascular endothelial cells by inhibiting the hypoxia activation of microglias, reducing the expression of TLR4 and gp91phox, and increasing the expression of ZO-1.

Meta-analysis of the effectiveness of Chinese and Western integrative medicine on medium and advanced lung cancer / 中国结合医学杂志

<p><b>OBJECTIVE</b>To summarize the effectiveness of Chinese and Western integrative medicine in treating medium and advanced lung cancer, and to provide guidelines for clinical application.</p><p><b>METHODS</b>For this metaanalysis, a comparative search of Chinese medicine data in Chinese National Knowledge Infrastructure (CNKI) and Chinese BioMedical Literature Database (CBM) was undertaken to identify articles related to randomized comparative research of Chinese and Western integrative medicine in treating medium and advanced lung cancer between 1996 to 2006. Quality of life (QOL) was estimated using RevMan 4.2 software for data processing, adopting the odd ratio (OR) and the 95% confidence interval (CI).</p><p><b>RESULTS</b>Through meta-analysis of 10 qualified articles, the results were as follows: the merging effectiveness of QOL [OR=3.80, 95% CI (2.65, 5.47)]; the rate of survival [OR=3.44, 95% CI (2.04, 5.80)]; the tumor response rate [OR=1.88, 95% CI (1.37, 2.58)]; the tumor developing rate [OR=0.33, 95% CI (0.23, 0.48)]. Significant differences existed between the Chinese and Western integrative medicine treatment group and the Western treatment group (P<0.01).</p><p><b>CONCLUSIONS</b>Chinese and Western integrative medicine treatment of medium and advanced lung cancer has shown to improve patients' QOL and survival rate; it also can control tumor development in the short term.</p>

Effect of effective components of huanglian jiedu decoction on hypoxia, reoxygenation injury and the expression of VCAM in cultured rat cerebral microvascular endothelial cells / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the protective mechanism of geniposide, baicalin and berberine on hypoxia and reoxygenation injury in cultured rat cerebral microvascular endothelial cells.</p><p><b>METHOD</b>A model of four hours hypoxia and twelve hours reoxygenation injury in rat cerebral microvascular endothelial cells in vitro was established. The injured cells were treated with geniposide (0.128, 0.064, 0.032 mmol x L(-1)), baicalin (0.028, 0.014, 0.007 mmol L(-1)) and berberine (0.024, 0.012, 0.006 mmol L(-1)), respectively. The immunocytochemical method and techniques of image quantitative analysis were used to detect the mean optical density and mean area in order to match the protein expression of VCAM-1. The method of RT-PCR was adopted to observe and match the mRNA expression of VCAM-1.</p><p><b>RESULT</b>As compared with the normal group, the mean optical density, the mean area and the mRNA expression of VCAM-1 of model group were significant increased (P < 0.01, P < 0.01, P < 0.01). As compared with the model group, both the mean optical density and the mean area of all treated groups were decreased, and there was significant difference between them (P < 0.01, P < 0.01). As compared with normal group, the mean optical density of baicalin (0.007 mmol x L(-1)) and berberine (0.012, 0.006 mmol x L(-1)) were significant decreased (P < 0.05, P < 0.01, P < 0.01), but there was no significant difference between the other groups and the normal group. As compared with normal group, the mean area of baicalin (0.0014 mmol x L(-1)) was significant decreased (P < 0.05), but there was significant difference between the other groups and the normal group. The mRNA expression of all treated groups was not only lower than that of the model group but also higher than that of the normal group (P < 0.05, P < 0.05).</p><p><b>CONCLUSION</b>The results suggest that geniposide, baicalin and berberine, which are effective compositions of huanglian jiedu decoting, can protect hypoxia-reoxygenation injuried rat cerebral microvascular endothelial cells. One of the protected mechanisms is that they can inhibit the expression of VCAM-1.</p>

Effect of effective components of Huanglian Jiedu decocting on NF-kappaB in cultured rat cerebral microvascular endothelial cells injury induced by hypoxia and reoxygenation / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the protective mechanism of geniposide, baicalin and berberine on hypoxia and reoxygenation injury in cultured rat cerebral microvascular endothelial cells.</p><p><b>METHOD</b>To establish a model of hypoxia four hours and reoxygenation twelve hours injury in rat cerebral microvascular endothelial cells in vitro. The injured cells were treated with geniposide (0. 128, 0.064, 0.032 micromol mL(-1), baicalin (0.028, 0.014, 0.007 micromol mL(- 1)) and berberine (0.024, 0.012, 0.006 micromol mL(-1)). The expression of p65 subunit of NF-kappaB was detected by immunocytochemical assay and techniques of image quantitative analysis. The protein expression of NF-kappaB was calculated with the mean optical density and mean area. The nuclear translocation of NF-kappaB was calculated with the percentage of positive cells and ratios of light transmittance of cytoplasm and cell nucleus.</p><p><b>RESULT</b>Compared with the normal group, both the protein expression and the nuclear translocation of NF-kappaB of model group were significant increased (P <0.01). Compared with the model group, the mean optical density of all treated groups was decreased ,but these was no significant difference between them. As compared with model group, the mean area of all treated groups was significant decreased (P < 0.01). The percentage of nuclear translocation of all treated groups is not only lower than that of the model group but higher than that of the normal group (P <0.01). Compared with the model group, the ratios of light transmittance of cytoplasm and cell nucleus of all treated groups was significantly elevated (P <0.01).</p><p><b>CONCLUSION</b>The results suggesed that geniposide, baicalin and berberine could protect hypoxia/reoxygenation injuried rat cerebral microvascular endothelial cells injury. One of the mechanism may lie in inhibiting both the protein expression and the nuclear translocation of NF-kappaB.</p>

Protective action of effective components of Huanglian Jiedu decoction on hypoxia and reoxygenation injury in cultured rat cerebral microvascular endothelial cells / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the protective effect of geniposide, baicalin and berberine for the rat cerebral microvascular endothelial cell.</p><p><b>METHOD</b>The model of hypoxia and reoxygenation injury in rat cerebral microvascular endothelial cells in vitro was established. Both normal and model cells were treated with geniposide (1.024, 0.512, 0.256, 0.128, 0.064, 0.032, 0.016, 0.008 micromol x mL(-1)), baicalin (0.224, 0.112, 0.056, 0.028, 0.014, 0.007, 0.003 micromol x mL(-1)) and berberine (0.192, 0.096, 0.048, 0.024, 0.012, 0.006, 0.003 micromol x mL(-1)). Cell activity was measured by methyl thiazolyl tetrazolium (MTT) test.</p><p><b>RESULT</b>After hypoxia/hypoglycemia cultures for 4 hour and reoxygenation for 12 hour, geniposide (0.128, 0.064, 0.032 micromol x mL(-1)), baicalin (0.028, 0.014, 0.007 micromol x mL(-1)) and berberine (0.024, 0.012, 0.006 micromol x microL(-1) could protect the injuried cerebral microvascular endothelial cells.</p><p><b>CONCLUSION</b>Appropriate concentration of geniposide, baicalin and berberine, which are effective components of Huanglian Jiedu decoction, could protect the injuried cerebral microvascular endothelial cells.</p>

The protective effect of cholic acid on an in vitro injury model of ischemia-reperfusion in cerebral microvascular endothelial cells / 中国中药杂志

<p><b>OBJECTIVE</b>To establish an in vitro injury model of ischemia-reperfusion in cerebral microvascular endothelial cells of rats and observe the protective effect of cholic acid.</p><p><b>METHOD</b>Cultured rat microvascular endothelial cells were subjected to the oxygen-glucose deprivation (OGD) (Krebs solution) and recovery of oxygen-glucose, which simulated in vitro ischemia and reperfusion injury, and treated with cholic acid. The A value was measured with MIT chromatometry.</p><p><b>RESULT</b>Cultured cells were impaired after OGD for 4 hours and recovery of oxygen-glucose for 12 hours, the A value of the cells treated with cholic acid was significantly higher than that of the cells without treatment (P < 0.01).</p><p><b>CONCLUSION</b>Cholic acid could obviously protect rat cerebral microvascular endothelial cells from injury induced by an in vitro ischemia-reperfusion.</p>