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??OBJECTIVE To discuss the effect and mechanism of supplementing qi and nourishing yin(SQNY) decoction on intestinal microbiome of mice with Lewis lung carcinoma after treated with cisplatin. METHODS The model of C57BL/6 mice with lung carcinoma xenograft was established by subcutaneous seeding of Lewis cells and randomly divided into 4 groups (n=16), including saline group (NC group), cisplatin group (DDP group), CAP group (CAP group) and SQNY decoction combined with cisplatin group (DDP+SQNY group). The tumor sizes, weights and intestinal microbiota were detected. The serum levels of IL-6, IL-10, and TNF-?? were detected by ELISA. The dendritic cell (DC) and macrophage subtype in spleen of mice models were detected by flow cytometry. RESULTS ??The mean tumor sizes of mice in DDP group, CAP group, DDP+SQNY groups were all smaller than NC group (P<0.05). And the mean tumor size and weight in DDP+SQNY group were less than the other three groups (P<0.05). The mean animal weights in NC or DDP+SQNY group were higher than those in DDP group and CAP group (P<0.05). ??The mean levels of serum IL-6, IL-10 and TNF-?? in DDP+SQNY group were less than those in the other three groups (P<0.05). ??The mean microbiota richness in DDP+SQNY group were less than those in the other three groups (P<0.05). The proportion of fecal microbiota was significantly changed in DDP+SQNY group, including upregulation of Firmicutes phylum and Bifidobacterium Genus, and downregulation of Bacteroidetes phylum(P<0.05). ??The amount of DC and M1/M2 macrophage subtype in spleen of DDP+SQNY group mice models were more than those in the other three groups (P<0.05). CONCLUSION It??s suggested that SQNY decoction effectively enhances the anticancer effect of cisplatin by increasing the immune function and changing the intestinal microbiota.     

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??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.     

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??OBJECTIVE To investigate the anti-proliferation effects of andrographolide Derivative(ADA) and its potential anti-tumor mechanisms in MCF-7 cells. METHODS The anti-proliferation effects of ADA were assessed by MTT assay in MCF-7 cells. Apoptotic morphological changes of MCF-7 cells after ADA treatment were observed by high content screening (HCS) after AO/EB double staining and DAPI, Apoptotic number was investigated by using flow cytometry. The expression of Bcl-2, Bax,caspase 3,NF-??B p65,p-I??B?? and p-IKK?? were measured using Western blot.RESULTS MTT assay demonstrated that ADA exerted potent anti-tumor effect in a significant concentration-dependent manner;ADA could promote the apoptosis of MCF-7 cells. Western blot results showed that Bcl-2 families and NF-??B p65 and caspase 3 involved in the process of apoptosis, Bcl-2 expression lowered(P<0.05),p-I??B?? and p-IKK?? expression decreased(P<0.01), Bax, NF-??B p65 and caspase 3 expression increased(P<0.01). CONCLUSION ADA could inhibit the proliferation of MCF-7 cells and mechanism may be that it might induce apoptosis by regulated the expression of Bax, Bcl-2 and caspase 3 protein and NF-??B passway.     

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??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.     

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??OBJECTIVE To investigage the effects of celastrol-triggered HeLa cells autophagy and the molecular mechanisms in vitro and in vivo. METHODS The antiproliferative effect of celastrol was detected using MTT assay. Apoptotic rate and cell cycle were evaluated using flow cytometric analysis. Autophagy was detected using fluorescence microscope. Protein expression was evaluated using Western blotting. Tumor growth was evaluated by subcutaneous xenograft model in vivo. RESULTS Celastrol inhibited HeLa cells proliferation and induced HeLa cells autophagy and cell cycle arrest at G₀/G₁ phase, but not induced HeLa cell apoptosis in vitro. The protein expression of Beclin 1 was up-regulated and the conversion from LC3 ?? to LC3 ?? was increase in HeLa cells in vitro after treatment with celastrol. Moreover, celastrol promoted the protein expression of PTEN??p-ERK1/2??p-MEK1/2 and inhibited the phosphorylated of Akt, p70S6K and mTOR in HeLa cells. After pretreatment with 3-methyladenine (5 mmol??L^-1), the antiproliferative and induced-autophagy effects of celastrol were reversed. Furthermore, celastrol inhibited tumor growth and the protein expression of p-Akt and p-mTOR, but up-regulated the protein expression of LC3 ?? and Beclin 1 in vivo. CONCLUSION Antitumor effect of celastrol dependent on cells autophagy in HeLa cells via inhibition of Akt/mTOR signaling pathway in vitro and in vivo.     

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??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.     

魟鱼软骨多糖对小鼠Lewis肺癌的作用及分子机制探讨

目的:研究魟鱼软骨多糖(RCG)对小鼠Lew is肺癌的作用,并初步探讨其作用机制。方法:建立小鼠Lew is肺癌模型,将实验分为生理盐水(Saline)组、不同剂量魟鱼软骨多糖(RCG)组、环磷酰胺(CTX)组,计算原发瘤抑制率及肺转移数;采用RT-PCR和W estern b lot检测原发瘤组织VEGF、bFGF mRNA和蛋白表达。结果:应用魟鱼软骨多糖各剂量组,小鼠原发瘤抑制率、肺转移数与生理盐水组比较差异有显著性(P<0.05,P<0.01);与生理盐水比较,魟鱼软骨多糖各剂量组,VEGF、bFGF mRNA和蛋白表达水平显著降低(P<0.01)。结论:魟鱼软骨多糖明显抑制小鼠Lew is肺癌原发瘤的生长和转移,可能与其抑制肿瘤VEGF、bFGF mRNA和蛋白表达有关。