樟树 枳壳走快价扬栀子货丰价跌

春节临近,入市购买药材的人员日渐增多,本期市场上滋补类和香料类药材商品交易显得较为活跃,小批量零星交易走快。丹参、板蓝根、白术等大宗品种交易量明显上升,价格有上扬之势,一些冷背品种如重楼、香薷草、皂角等因货源短缺,价格上涨幅度较大。现将部分地产果实子仁类药材行情走势点评如下:枳壳江西是主要产区,历年年产量均占全国的五成以上,主产于本省的中南部,其中樟树、新干、新余、吉水、高安、峡江、安福、万载、永新、吉安等市县拥有大型的GAP生产基地。地产枳壳以其皮青肉厚的品质深受药厂、药商的青睐,因此,前些年商品走动比较顺畅。进入2003~2004年,随着产地种植面积增加,枳壳产量逐年上升,加上受湖南、湖北等地枳壳价低的影响,江西枳壳价格开始逐步下滑,统货成交价陆续降至6~6.5元(千克价,下同),低谷时只有5元,产地药农因收入不佳于是放松了对枳壳树的管理,有的地方甚至砍伐树木改种其它作物,由此导致枳壳面积逐步减少,产量也逐年下降。近两年受自然灾害的影响,加上产地外出务工人员增多,枳壳采摘量明显减少,而近年来随着相关制药企业对枳壳新产品的开发利用其商品市场需求量不断增加。2006年因货源减少价格开始回升。2007年枳壳商品...     

黄养民治疗妇科疾病经验

黄养民(1904-1985),湖北武昌人.出生在中医世家,黄师悉得先父真传,后又拜妇科名医张金山为师.随师9年,继承了张师妇科药物炮制和内服以及局部用药的经验,给黄师后来医治妇科疾病打下了坚实基础.抗日战争时期,参加抗日救护队.后逃难到重庆北碚,考入中医救急医院任医生,继续进行难民的救护活动.     

谱写最神奇的生命旋律

前不久,在美国百老汇举行了一场音乐晚会,奇怪的是,舞台上空空荡荡,不见一件乐器。首先登台表演的是一名看起来没有多少艺术气质的彪形大汉,只见他做了个威猛的亮相后,就开始脱掉外衣,裸露出他那身浑厚而又刚健的肌肉,并开始将身体剧烈地抖动起来,     

枳壳走快价扬 栀子货丰价跌

进入2008年,市场大货交易仍不多见,以中小批量货源走动为主。防己、天花粉、石菖蒲、怀牛膝、壳砂、莱菔子、菟丝子、肉豆蔻、公丁香、五倍子等价格上升,麦冬、云木香、泽泻、栀子等价格下滑。白茅根又名寒草根、甜草根等,有性寒,具有凉血,止血,生津止渴,清热利尿等功效,是药材中的小三类品种,全国各地均有生长。以前植被资源保护较好,河边滩涂、田间地头多生长白茅根,每到冬闲季节农民多去采挖,或做柴烧、或当作药材卖掉换零用钱。目前正是白茅根集中上市季节,但市场缺少大货,优质货市价已升到7~8元(千克价,下同),这个不起眼的小品种,后市引起了商家的注意。造成其价格上升的主要原因:一是由于环境污染、河道治理,使白茅根生长环境受到破坏,其野生资源不断减少;二是劳动力价值提高,青壮年劳动力多外出打工,采集白茅根的人越来越少;三是白茅根以野生为主,目前还没有人工种植,野生资源减少,而没有人工种植的补充,所以市场货源越来越少;四是物价上涨也是带动其价格上升的因素。金银花在医药、保健食品、化妆品等方面需用量较大,主产山东、河南、河北、湖南等地。2003年的“非典”把金银花带到了历史的高价,后又下滑。2007年由于受自然因素的影响,山东、...     

马融教授运用三仁汤治疗儿科疾病验案3则

三仁汤出自<温病条辨-上焦篇>,系吴鞠通专为湿温初起而设,由苦杏仁、白豆蔻、薏苡仁、滑石、通草、竹叶、半夏、厚朴组成,旨在宣畅气机、清利湿热.导师马融教授是天津中医药大学第一附属医院著名儿科专家,其认为只要充分把握三仁汤的方证特点,对于病程迁延、面色萎黄、胸满纳呆、舌苔黄厚腻者,临床可广为使用,不必拘于湿温初起.现将验案介绍如下.     

对青黛临床应用中的几点建议

青黛是临床常用的具有清热解毒、凉血功效和抗癌作用的中药,然由于青黛在其加工制备过程中常夹有一定量的石灰,在临床的内服或外用时,对机体产生刺激的副作用,且降低青黛本身的临床效果,干扰和影响复方中其他药材中成分的溶出.况青黛本身质轻易浮,不溶于水,入煎剂或凉开水调敷外用时,常使疗效降低,浪费药材.     

血府逐瘀汤皮肤科临床应用一得

血府逐瘀汤出自王清任的《医林改错》，方由当归、生地、桃仁、红花、柴胡、枳壳、牛膝、川芎、赤芍、甘草、桔梗组成，具有活血祛瘀、行气止痛功效。笔者运用此方治疗各种皮肤病，取得良好的效果。现举例介绍如下。     

姜德友辨治消渴重症验举隅

姜德友教授系黑龙江中医药大学名中医,师从全国名老中医张琪教授,从事中医临床、科研工作20余年,学验俱丰,对糖尿病合并心肌病、冠心病、肝炎、肾病诊治较有心得,擅用经方治疗疑难杂症,每起沉疴.笔者、有幸随师侍诊多年,现择出老师诊治之消渴危重病案,以飨读者.     

HPLC法分析甘草芫花合煎液与合并液成分

目的对甘草芫花合煎液和合并液进行HPLC测定,分析两种提取液色谱图差异,探讨甘草芫花配伍产生毒性的可能机理.方法制备甘草芫花提取液、甘草芫花合煎液及1∶ 1合并液,分别进行HPLC测定.结果甘草芫花合煎液与合并液色谱图存在一定差异,合并液色谱图与芫花色谱图在12 min均有一个吸收峰,而合煎液的色谱图没有发现类似峰,但在10.5 min出现一个新的吸收峰,此吸收峰在甘草与芫花的色谱图中均未发现.结论甘草芫花合并煎煮与分别煎煮后成分具有差异,这种差异同甘草与芫花的配伍合理性之间存在的关系,以及因煎煮工艺不同而造成毒性程度的不同等问题,值得进一步研究.     

ȹ���˶����������յ��˸ΰ�HepG-2ϸ�����������о�

??OBJECTIVE To investigate the mechanism of human liver cancer HepG-2 cells apoptosis induced by Undaria pinnatifida sulfated polysaccharides S-UPPS??B. METHODS The anti-proliferation effects of S-UPPS??B on HepG-2 cells was by MTT assay. [Ca²⁺]i in HepG-2 cells was detected by laser cofocal scaning microscopy (LCSM). The apoptosis rate and protein expression level of Bcl-2, Bax, Cyt-C and p53 were detected by flow cytometry (FCM). Caspase Assay Kit was used to detected the activities of Caspase-3 and -9. RESULTS S-UPPS??B could inhibit the proliferation of HepG-2 cells and the IC₅₀ was 50.09 ??gmL^-1. With the increase of drug delivery dosage, apoptosis rate also increased, and the significant regulating effects of S-UPPS??B on Ca²⁺ and its associated channel proteins were observed. The [Ca²⁺]i level, the protein expression level of Cyt-c, p53 and the activities of Caspase-3 and -9 were all increased remarkably (P<0.05). The ratio of Bcl-2 to Bax was reduced. CONCLUSION Undaria pinnatifida sulfated polysaccharides S-UPPS??B can effectively inhibit the proliferation of human liver cancer HepG-2 cells by inducing apoptosis of HepG-2 cells through mitochondrial pathway.     

����ľ������ͨ���������PI3K/AKTͨ·�յ�MCF-7ϸ���������о�

??OBJECTIVE To study the effect of isoalantolactone on inhibiting proliferation of MCF-7 and induce apoptosis in vitro and further to explore its machinism via mitochondrial and phosphatidylinositol 3-kinase/Akt signaling pathways. METHODS The subject investigated isoalantolactone in MCF-7 cells proliferation inhibition by MTT and SRB methods, and matching the results of two methods; observing morphological changes by inverted microscope and each phase of apoptosis of MCF-7 cells effected by isoalantolactone after 24 h with Hoechst 33258 staining method. Using transmission electron microscopy to observe MCF-7 cells morphology change to determine the mechanism of research; rhodamine 123 tag, laser confocal scanning microscope detection isoalantolactone on the effect of MCF-7 cells mitochondrial membrane potential; Using Western blot to the expression of Bcl-2,Bax,Akt and p-Akt; detecting caspase-3 activity in MCF-7 cells by colorimetry method. RESULTS Isoalantolactone has strong inhibition of proliferation in MCF-7 cells, IC₅₀ values of MTT and SRB methods were 15.21 and 14.908 ??g??mL^-1, and in a dose -dependent manner; the morphological of MCF-7 cells was changed after the treatment by Hoechst staining method; morphological changes were observed under transmission electron microscopy of cells display, the drug group cells showed typical apoptotic characteristics of different periods. With the concentrations of isoalantolactone increasing, the level of mitochondrial membrane potential reduced. Western blot result showed that, isoalantolactone could down regulate the expression of anti apoptotic protein Bcl-2, p-Akt, and up regulate the expression of pro-apoptotic protein Bax, had no effect on the expression of Akt protein. And the activity of caspase-3 could be raised by increasing dosage, compared with the control group with significant difference(P<0.01). CONCLUSION Isoalantolactone effectively inhibites the proliferation of MCF-7 cells through mitochondrial and phosphatidylinositol 3-kinase/Akt signaling pathways, which is regulated by activation of caspase-3, down-regulation of Bcl-2, and up-regulation of Bax. Isoalantolactone-induced apoptosis is involved in mitochondrial and the PI3K/Akt pathway.     

˫���������յ��˸ΰ�ϸ��SMMC-7721����������ӻ����о�

??OBJECTIVE To investigate the apoptosis effect of human hepatocellular carcinoma cell line SMMC-7721 induced by dihydroartemisinin in vitro and the possible mechanism. METHODS After treatment with 25, 50, 100, 200, and 400 ??mol??L^-1 dihydroartemisinin for 24 h. The proliferation inhibitory effect of dihydroartemisinin on SMMC-7721 cell was detected by MTT assay. Cell cycle and apoptosis were detected by flow cytometry. The change of apoptotic morphology was detected by confocal laser scanning microscopy. Rho 123 staining method was used to detect the changes of mitochondrial membrane potential. Western blot was used to detect expression of Bcl-2, Bax, Cleaved Caspase-3, Cleaved Caspase-9 and Cyto C. RESULTS MTT results showed that 25-400 ??mol??L^-1 dihydroartemisinin can inhibit the proliferation of SMMC-7721 cells obviously. The cell cycle detection results of flow cytometry showed that dihydroartemisinin could block SMMC-7721 cell cycle in G₂/M phase. The results of Hochest 333258 staining showed that the nuclei were heterogeneous, condensed and fragmented in the DHA treatment group. The cell apoptosis detection results of flow cytometry showed that the apoptosis rate of dihydroartemisinin treated groups were increased obviously (P<0.01). The results of Rho 123 staining showed that the mitochondrial membrane potential was decreased significantly (P<0.01). Western blot results showed that the expression of Bcl-2 was down-regulated, expression of Bax was up-regulated, the ration of Bax/Bcl-2 was increased and the expression of Cleaved Caspase-3, Cleaved Caspase-9 and Cyto C were up-regulated. CONCLUSION Dihydroartemisinin can induce apoptosis of SMMC-7721 cells, on the mechanism of apoptosis may be related to mitochondrial pathway.     

��������ˮ����Զ�������յ�H9c2ϸ������������Ӧ������������

??OBJECTIVE To study the protective effects and mechanisms of aqueous extract from Descurainia sophia on doxorubicin(Dox)-induced cardiomyocyte injury.METHODS The Dox induced H9c2 cell apoptotic model was established, then the cells were divided into normal group (NC), model group (Dox), positive group (resveratrol,RSV), and different doses of aqueous extract of Descurainia sophia (DS). The viability of H9c2 cells was detected by MTT assay. The apoptosis rate, mitochondrial membrane potential and reactive oxygen species (ROS) level were detected by flow cytometry. The levels of T-SOD, LDH, MDA and GSH-PX were measured. And the protein expression levels of caspase-3, Bcl-2, Bax and p53 were detected by western blot, HPLC-MS identification of aqueous extract from Descurainia sophia.RESULTS After treating with DS products, the survival rate of H9c2 was increased (P<0.01), the apoptosis rate was significantly decreased (P<0.01),mitochondrial membrane potential was significantly increased (P<0.01), the level of ROS was significantly decreased (P<0.05), T-SOD and GSH-PX activities were significantly increased (P<0.01), the levels of LDH and MDA content were significantly decreased(P<0.01). Moreover, DS reduced the expression of caspase-3 (P<0.01), regulated the expression of Bax/Bcl-2 (P<0.01), decreased the expression of p53 (P<0.05). Seven components were identified from DS by HPLC/MS analysis.CONCLUSION DS can effectively protect cardiomyocyte, and its mechanism is probably associated with correcting functional disorders of oxidative stress of cardiomyocytes, and inhibit mitochondrial apoptotic pathway.     

��ϸ�����������յ�������ϸ���԰�Ѫ��K562ϸ��������ЧӦ�о�

??OBJECTIVE To investigate the protection of hepatocyte growth factor (HGF) on CML cell line K562 from apoptosis induced by etoposide (VP-16) and its molecular mechanism. METHODS Quantitative and qualitative analyses on cell morphological change of apoptosis were performed through acridine orange (AO) staining and HE staining, and fluorescent flow cytometry.The test analyzes membrane on the surface of the PS evagination and integrity of cell membrane surface and mitochondrial membrane potential changes were performed through Annexin V-FITC/PI double dyeing and JC-1 cell dyeing tests, and apoptotic factors such as Bcl-2, Bax, Caspase-3 and Caspase-9 were measured by SYBR Green (Takara) qRT-PCR. RESULTS The HE and AO staining revealed that apoptotic rates in HGF+VP-16 groups were significantly lower than those in VP-16 groups (P<0.05,P<0.05), HGF can inhibit the apoptosis of cells induced by VP-16; FCM (Annexin V-FITC/ PI and JC-1) tests showed that cells apoptotic rates in HGF+VP-16 groups were significantly lower than those in VP-16 groups (P<0.05,P<0.001), indicating that HGF has the anti-apoptosis function. Apoptosis related gene mRNA expression tests found that the Bcl-2 mRNA expression in HGF+VP group was obviously higher than that in the VP-16 group (P<0.001), while Bax mRNA, Caspase-3 mRNA, and Caspase-9 mRNA expressions were significantly lower than those in the VP-16 group (P<0.05, P<0.001, P<0.001),suggesting that HGF possesses antiapoptotic effect through inhibiting apoptosis gene expression and promoting the antiapoptotic gene expression simultaneously. CONCLUSION HGF can significantly protect K562 cells from apoptosis induced by VP-16 through the HGF/c-Met way to regulate PI3K/AKT pathway.     

Dehydrocorydaline inhibits breast cancer cells proliferation by inducing apoptosis in MCF-7 cells

Dehydrocorydaline is an alkaloid isolated from traditional Chinese herb Corydalis yanhusuo W.T. Wang. We discovered that it possessed anti-tumor potential during screening of anti-tumor natural products from Chinese medicine. In this study, its anti-tumor potential was investigated with breast cancer line cells MCF-7 in vitro. The anti-proliferative effect of dehydrocorydaline was determined by MTT assay and the mitochondrial membrane potential (Δ Ψ m) was monitored by JC-1 staining. DNA fragments were visualized by Hoechst 33342 staining and DNA ladder assay. Apoptotic related protein expressions were measured by Western blotting. Dehydrocorydaline significantly inhibited MCF-7 cell proliferation in a dose- dependent manner, which could be reversed by a caspase-8 inhibitor, Z-IETD-FMK. Dehydrocorydaline increased DNA fragments without affecting ΔΨm. Western blotting assay showed that dehydrocorydaline dose-dependently increased Bax protein expression and decreased Bcl-2 protein expression. Furthermore, dehydrocorydaline induced activation of caspase-7,-8 and the cleavage of PARP without affecting caspase-9. These results showed that dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.     

�����ͨ��������;���յ����ѳ���ϸ������

??OBJECTIVE To study the effect of toosendanin (TSN)on the apoptosis of human ovarian cancer cell and to clarify the related mechanism. METHODS CAVO-3 and A2870 cells were treated with toosendanin of different concentrations, and CCK-8 method was used to detect the cell survival rate, colorimetric method was used to measure the activities of Caspase-3 and Caspase-9, EdU method was used to determine the cell proliferation rate, and Western blot method was used to test the expressions of Bcl-2, Bax and Cyto-C protein. RESULTS TSN could significantly inhibit the survival of CAVO-3 and A2870 cells with dose-(r=0.869 1, P<0.05) and time-(r=0.776 5, P<0.05) dependent manners. The survival rate of A2870 cell with TSN dropped significantly (P<0.05). The activities of Caspase-3 and Caspase-9 were significantly increased by TSN in CAVO-3 and A2870 cells, however, the inhibitors of Caspase-3 (z-DEVE-FMK) and Caspase-9 (z-LEHD-FMK) could reverse those effect of TSN (P<0.05) and also reverse the survival rates of CAVO-3 and A2870 cells (P<0.05). In addition, TSN could increase the expression of Bcl-2, Bax and Cyto-C protein in A2870 cells notably, which could be reversed mostly by Caspase-9 inhibitor (z-LEHD-FMK)(P<0.05). CONCLUSION TSN could induce the apoptosis in human ovarian cancer cell through up-regulating the activities of Caspase-3 and Caspase-9, and then activates the mitochondrial pathway.     

��������֬�����յ�θ��BGC-823ϸ��������ʵ���о�

??OBJECTIVE To study the apoptosis of human gastric cancer cell line BGC-823 induced by liposome of total glucosides from paeonia(TGP liposome ). METHODS The inhibition of cell proliferation was determined by Cell Counting Kit-8 assay.The morphological changes of the apoptosis cells were observed by HE staining,Hoechst 33258 fluorescent staining, transmission electron microscope. Changes of apoptosis related factor Bcl-2 and Bax protein expression were detected by Western blot. RESULTS TGP liposome significantly inhibited proliferation of BGC-823 cells in a dose-dependent manner(P<0.05). GC-823 cells induced by TGP liposome for 48 h was observed on morphological changes such as karyopyknosis and karyorrhexis and apoptotic bodies. Bcl-2 expression was reduced, but Bax expression was increased,so the ratio of Bcl-2 /Bax decreased. CONCLUSION TGP liposome can induce the apoptosis of BGC-823 cells and inhibit its proliferation, its mechanism may be related to down-regulating protein expression of Bcl-2, up-regulating protein expression of Bax, reducing Bcl-2/Bax value.