目的:分析红景天苷(Sal)对小鼠原代T淋巴细胞体外行为的影响.方法:无菌分离并培养BALB/c近交系小鼠淋巴结细胞,MTT比色法检测并分析Sal对小鼠T淋巴细胞活力的影响;荧光染料标记的单克隆抗体染色结合流式细胞术(FCM)检测刀豆蛋白A(Con A)诱导作用下Sal对T淋巴细胞活化抗原CD69表达水平的影响.羧基二乙酸荧光素琥珀酰亚胺酯(CFDA-SE)染色分析T淋巴细胞体外增殖情况.2',7'-二氯二氢荧光素二乙酸酯(H2DCFDA)荧光染色检测小鼠T淋巴细胞胞内活性氧簇(ROS)生成.DiOC6(3)染色检测Sal对T淋巴细胞胞内线粒体活性的影响以及地塞米松(DEX)诱导作用下Sal对T淋巴细胞线粒体膜电位的影响.制备小鼠胸腺T淋巴细胞悬液,FCM检测DEX诱导作用下胸腺T淋巴细胞的凋亡率.结果:终浓度为80、160和320μmol/L的Sal均能提高T淋巴细胞活化抗原CD69的表达水平(P<0.05).Sal能促进Con A诱导72 h条件下T淋巴细胞体外增殖(P<0.01),且能减少T淋巴细胞胞内ROS生成量(P<0.05),对T淋巴细胞线粒体膜电位有保护作用(P<0.01).Sal能明显降低DEX诱导条件下的胸腺T淋巴细胞凋亡率(P<0.01).结论:Sal能够促进T淋巴细胞的体外活化和增殖,减少T淋巴细胞内ROS的产生,维持细胞内线粒体膜电位稳定性,抑制DEX诱导条件下胸腺T淋巴细胞的凋亡.

BACKGROUND:Because macrophages play an important role in the body’s inflammatory response, the detection of the impact of biological materials on the behavior of macrophages can assess the immunogenicity of materials. OBJECTIVE: To analyze the activation effect of decelularized extracelular matrix materials on macrophages. METHODS: The peritoneal macrophages of BALB/c mouse were obtained and cultured by dividing into five groups. Control group was simple cel culture group, experimental group 1 was acelular matrix membrane material directly contacting with macrophage for culture, experimental group 2 was fresh pericardial material directly contacting with the macrophage for culture, experimental group 3 was acelular matrix membrane material indirectly contacting with macrophages for culture, experimental group 4 was fresh pericardium material&nbsp;indirectly contacting with macrophages for culture. After 24 hours of culture, the secretion of nitric oxide and cytokines in cel culture supernatant was determined. After 48 hours of culture, the absorbance value was determined by MTT method and the toxicity grading was determined. RESULTS AND CONCLUSION: The toxicity grading in experimental groups 1-4 was respectively grades 2, 4, 0, 2. The nitric oxide level in experimental groups 1 and 2 was higher than that in the control group (P < 0.05), and the nitric oxide level in the experimental group 2 was higher than that in the experimental group 1 (P < 0.05). There were no significant differences in interleukin-2, interleukin-4,interferon γ, interleukin-17A and interleukin-10 levels between these five groups. The interleukin-6 level in the experimental group 2 was higher than that in the control group (P < 0.05); The expression levels of tumor necrosis factors in experimental group 1, 2 and 4 were higher than those in the control group (P < 0.05), and experimental group 2 higher than the experimental group 1 (P < 0.05), experimental group 1 higher than the experimental group 4 (P < 0.05). These results show that acelular matrix material can activate macrophages in direct contact.

[ ABSTRACT ] AIM: To observe the effect of rapamycin on the apoptosis of mouse astrocytes in vitro.ME-THODS:The astrocytes from C57BL/6J newborn mouse pups were isolated and primarily cultured.The effect of rapamycin on the viability of astrocytes was assessed by MTT assay.The mean fluorescence intensity of SYTOX?Green stain in the astrocytes was detected by fluorescence microplate reader in order to analyze the effects of rapamycin on the cell death in-duced by H2 O2 , ionomycin and/or deferorxamin.DiOC6 (3) staining was used to analyze the mitochondrial membrane po-tential of the astrocytes induced by H2 O2 .Flow cytometry analysis was used to determine the production of ROS in the as-trocytes and mitochondria by staining with H2 DCFDA and MitoSOXTM Red reagent, respectively.RESULTS: Rapamycin at concentration of 0.5 μmol/L protected the astrocytes against cell death induced by H2 O2 or deferoxamine plus ionomy-cin.Rapamycin protected the mitochondrial membrane potential of astrocytes from the injury of H2 O2 .It also reduced the production of ROS in the astrocytes and decreased the level of ROS in the mitochondria.CONCLUSION:Rapamycin re-duces the ROS overload in the mitochondria, keeps mitochondrial membrane potential safety and protects the astrocytes a-gainst apoptosis in vitro.

目的:探讨灭活的1型人类免疫缺陷病毒颗粒(HIVp)对人小胶质细胞钙离子内流和转录因子NF-κB核转位的作用,对比不同亚型(HIVp-X4型与HIVp-R5型)的灭活HIVp所引发的钙离子内流强度差异.方法:将小胶质细胞接种到网形盖玻片上,用钙离子探针Fluo-4进行染色,用共聚焦显徼镜以荧光强度为指标实时观察不同刺激条件下细胞内钙离子水平的变化;联合胞内染色技术,用共聚焦显微镜记录不同处理条件下的小胶质细胞NF-κB核转位.结果:共聚焦显微镜检测结果显示HIVp所引发的钙内流效应明显强于gp120;在gp120同时存在的情况下,HIVp激发的钙离子内流效应会被其部分阻断;另外,HIVp-X4所引发的钙离子内流和NF-κB核转位要比HIVp-R5明显.结论:HIVp表面既有自身基因组编码的gp120蛋白,又有出胞时所携带的宿主蛋白,由于HIVp引发的钙内流效应明显强于gp120,因而推测HIVp表面的宿主蛋白在活化小胶质细胞中起了一定的协同作用;而HIVp-X4对小胶质细胞的刺激性明显强于HIVp-R5,提示X4型病毒是HIV相关性失智症的重要致病因素.

This study was conducted to explore the effects of AT-2-inactivated HIV-1 particles on the proliferation, apoptosis and tight junction of HT-29 cells. HIV-1IIIBparticles were inactivated by AT-2 chemical and then added to HT-29 culture system in optimal concentration. The proliferation and Ki-67 expression of HT-29 was evaluated by WST-1 assay and flow cytometry, respectively. The apoptosis of HT-29 was evaluated by Apo2.7 staining, as well as DIOC6(3) and NAO staining. Meanwhile, the tight junction of HT-29 was assessed by Occludin staining. Data showed that the proliferation of HT-29 was inhibited by AT-2-inactivated HIV-1IIIB particles. In addition, AT-2-inactivated HIV-1IIIBparticles induced HT-29 apoptosis, and disrupted the tight junction of HT-29. The results indicated that AT-2-inactivated HIV-1IIIBparticles strikingly affected the proliferation, apoptosis and tight junction of HT-29 cells, which means besides its immunopathogenicity, the cytopathogenicity of HIV-1 virion contributes to the intestinal pathogenesis of AIDS. The increased intestinal permeability might result in gut bacteria translocation, which then triggers systemic immune hyperactivation.

Before the technique of advanced high-throughput sequencing comes up , less is known about the human gut microbiota .It has been understood that trillions of microbes , in which 99% are bacteria , inhabit the human gut, forming a complicated ecological community .The gut microbiota has a great impact on human physiology and suscepti -bility to disease through its integrative metabolic activities and interactions with the host .In physiology , gut microbiota con-tributes to the host acquisition of nutrition and energy from diets , promoting development and maturation of gastrointestinal tract and immune system , and protecting host from invasion of enteropathogens .In pathology , dysbiosis underlying altered gut microbiota is associated with the susceptibilities to various diseases , including inflammatory bowel disease , type 1 dia-betes, asthma, obesity, metabolic syndrome , autism and cancer .Understanding of the factors that underlie alterations in the composition and function of gut microbiota will be helpful in the development of drugs and the design of therapies that target it.This goal is formidable .It is because that the compositions of gut microbiota are immensely diverse , varying be-tween individuals in a population and fluctuating over time in an individual , especially during early development and disea-ses.Viewing the gut microbiota with an ecological perspective will provide new insights into how to improve our health by targeting this microbial community in clinical treatments .

Mouse lymphocytes were isolated.The drug toxicology of different concentrations of AHI/ ICA on lymphocytes was measured by CCK-8 assay.The expression of CD69 and CD25,which were the markers of activation of T lymphocytes,was measured by FCM combined with two-color immunofluorescent staining of cell surface antigen.The proliferation of T lymphocytes was measured by FCM combined with live dye CFSE.The cell cycle of T lymphocytes was measured by FCM.The Calcium influx of T lymphocytes was measured by FCM’s time function.CBA kit was used to detect the production of cytokines of lymphocytes stimulated by con A.AHI and ICA decreased proportions of CD69 and CD25 on con A-stimulated lymphocytes in a dose-dependent manner.Both reduced the proliferation of T lymphocytes,and the influx of Calcium.AHI and ICA caused a G0 / G1 cell cycle arrest on con A-activated lymphocytes.Furthermore,both downregulated the secretion of cytokines(IL-6,IL-10,IFN-γ,TNF,IL12p70) of con A-activated lymphocytes.Furthermore,ICA exhibited more immunosuppressive effects than AHI on mouse T lymphocytes.

In this paper,the cytotoxiciy of DFO to lymphocytes was evaluated using MTT assay,carboxyfluorescein diacetatesuccinimidyl ester(CFDA-SE) staining plus flow cytometry assay was employed to investigate the effect of DFO on the proliferation of the lymphocytes,the expression levels of CD69 on T lymphocytes stimulated by Con A were evaluated with flow cytometry after staining with fluorescent monoclonal antibody,and Cell-cycle distribution of T lymphocytes was also analyzed by propidium iodide staining.The results showed that DFO induced-cytotoxicity had little impact on the reliability of our experiment data;DFO(5,10,20,40 μmol/L) significantly inhibited the proliferation of T lymphocytes stimulated by Con A for 48 h and 72 h;DFO at low concentrations(5,10 μmol/L) exerted no influence on the expression of CD69,however,DFO at high concentration(20,40 μmol/L) could inhibit the expression of CD69.The cell cycle distribution analysis revealed that DFO could induce a cell cycle arrest in G0/G1 phase.We can draw conclusion that DFO may use other mechanism except the inhibition of activation of T lymphocyte,to inhibit the proliferation of lymphocyte,it can induce a cell cycle arrest in G0/G1 phase.This effect demonstrates that DFO has the potential to be developed into a new immuo-intervention drug.

AIM: To explore the potential immunomodulatory effect and related mechanisms of ginkgolide B(GB),a known potent antagonist of platelet-activating factor receptor,on the pathological process of sepsis.METHODS: The experimental sepsis model was established by a standardized procedure of cecal ligation and puncture(CLP).GB treatment(10 μg/g) was given to the CLP mice 30 min before the surgical operation.The survival rate was observed every day for 3 weeks.The NO content in the serum was measured by Griess assay.The ROS level in the blood was determined by H2DCFDA labeling and flow cytometry.The inflammatory cytokines in the serum were detected by the methods of cytometric bead array and ELISA.RESULTS: The thymus and spleen of the mice significantly atrophied,and the levels of NO,ROS,TNF-α,IL-1β,IL-6 and IL-10 in the blood were dramatically elevated 24 h after CLP.All the CLP mice died in 5 days.However,treatment with 10 μg/g of GB 30 min before CLP remarkably enhanced the indexes of thymus and spleen,inhibited the storm of inflammatory mediators and cytokines,and improved the survival rate.CONCLUSION: The protective effect of GB on CLP-induced experimental sepsis indicates that GB is a candidate of natural immunomodulator for treating sepsis.

Objective To explore the effects of different culture systems on proliferation and differentiation of epidermal stem cells and to establish an optimal culture system which can regulate and control the proliferation and differentiation of epidermal stem cells.Methods The rat epidermal stem cells obtained by enzyme digestion and type Ⅳ collagen rapid adherence were cultured in different culture systems (culture on dish,co-culture with biological chitin scaffold material,and culture with chitin membrane as the carrier in nude mice).The growth of epidermal stem cells was then observed.After 4 weeks,the colonyformation rates of epidermal stem cells were compared among two systems (co-culture with biological chitin scaffold material and culture on dish).Immunohistochemistry was used to study the proliferation and differentiation of the epidermal stem cells with chitin membrane as a carrier in nude mice at 4 weeks after implantation.Results In routine culture dish,the epidermal stem cells began to proliferate and clone at around day 3 and fused into patches at around day 12.However,the proliferation gradually decreased and the time to fusing into patches gradually became longer after passage,until terminal differentiation and loss of proliferation after passages 3 to 4.In co-culture with biological chitin scaffold materials,the epidermal stem cells grew in a chessboard-like colony after 2 weeks,and a great number of colonies could be seen on the biological chitin scaffold materials,with plenty of proliferating cells adhering to the colonies.Under scanning electronic microscope (SEM),the biological chitin scaffold materials were found to mainly consist of fibers (10 μm in diameter) arranged in two crisscrossing layers with massive colonies of epidermal stem cells between the X-shaped holes.The epidermal stem cells cultured with biological chitin scaffold materials had a significantly higher colony forming efficiency as compared with that in culture dish after 4 weeks [ (12.6±2.7)％ vs (5.7± 1.1)％,P＜0.05 ].The epidermal stem cells implanted into the nude mice showed vigorous proliferation with formation of “epidermal nests” at 4 weeks after implantation.Structure of skin appendages could be seen around the nests of epidermal stem cells.Conclusions Epidermal stem cells can proliferate in the culture dish in vitro but remain proliferating only for a relatively short time.Co-culture with biological chitin scaffold materials may allow for longer-lasting proliferation of the epidermal stem cells.Massive proliferation can be found in the epidermal stem cells implanted into nude mice.

Objective To investigate the effects of ginsenoside Rb1 on activation and proliferation of murine T lymphocytes in vitro and to elucidate the mechanism of the immunosuppressive effect of ginsenoside Rb1.Methods Cell suspensions were prepared from murine lymph nodes.T lymphocytes were treated with different concentrations of ginsenoside Rb1 and stimulated with polyclonal activator concanavalin(ConA).Fluorescence conjugated monoclonal antibodies and flow cytometry were used to detect the expression of CD3/CD69 and CD4/CD25.After the staining with CFDA-SE,T lymphocytes were stimulated with polyclonal activator ConA.The proliferation of T lymphocytes,after stimulated by ConA,was detected using the method of MTT.The distribution of the cell apoptosis was analyzed by staining both DIOC and PI.Results In a dose-dependent manner,ginsenoside Rb1(5,10,and 20 μmol/L) could significantly inhibit T lymphocytes activation index(P0.01) stimulated by ConA and proliferation index(P0.05) stimulated by ConA.Ginsenoside Rb1 could also reduce the apoptosis of T lymphocytes stimulated by H2O2.Conclusion Ginsenoside Rb1 can effectively inhibit the activation and proliferation of murine T lymphocytes,and ginsenoside Rb1 is a potential effective immunoinhibitory agent.

This study aims to explore the effect of fisetin (FIS) extract on mouse T lymphocytes and the NO secretion of mouse macrophages further.We used Carboxyfluorescein diacetatesuccinimidyl ester (CFDA-SE) staining combined with flow cytometry assay to obtain the proliferation-related index (PI) of lymphocytes (72 h).The expression level of CD25 of T lymphocytes stimulated with Con A was evaluated with flow cytometry.In order to detect the change of the mitochondrial membrane potential,cells were stained with 3,3-dihexyloxacarbocyanine iodide [DiOC6 (3)].ROS production was monitored by flow cytometry using 2’,7’-dichlorodihydrofluorescein diacetate (H2DCFDA).Griess kit was used to evaluate the NO production of macrophages.Our results showed that fisetin (2.5 μmol/L,5 μmol/L and 10 μmol/L) significantly inhibited the proliferation of T lymphocytes.At the same time fisetin could obviously inhibit the expression of CD25 and the accumulation of ROS.We also found that the apoptosis of the lymphocytes could be accelerated by fisetin in the presence of dexamethasone (DEX).In addition,NO production of LPS plus IFN-γ-treated macrophages was clearly reduced by fisetin.These results indicate that fisetin might be a potential immunoregulation agent.

Aim: To investigate the protection effects of Bererine(Ber) on the thymocytes of middle cerebral artery occlusion-reperfusion(MCAO/R) injury mouse. Methods: The mouse model of focal cerebral ischemia reperfusion injury was induced by MCAO/R and was given 1.0 h occlusion and 24 h reperfusion.Three groups were randomly divided: Normal group,MCAO/R group which was given the same volume of solvent intraperitoneal injection(i.p.),and(MCAO/R + Ber) group,i.p.Ber with a concentration of 5 mg/kg,at 0.5 h ischemia and 12 h reperfusion separatively.After 24 h reperfusion,thymus was removed and thymus index was calculated,then thymocytes were harvested,fluorescence microplate reader and SYTOX Green dying were used to detect the cell activity,used AFM to find the cell morphology changes,and thymocytes early stage of apoptosis was tested by FACS and Calcein/CoCl2 dying or JC-1 staining. Results: MCAO/R led to serious thymus atrophy and a significantly lower thymus index(P<0.05).SYTOX Green staining reflected that MCAO/R injury induced higher cell mortality(P<0.05).AFM results indicated that notable changes of cell morphology,such as cell height reduced significantly(P<0.01),and rough rate increased remarkably(P<0.05).Calcein/CoCl2 and JC-1 dying showed that cerebral ischemia/reperfusion resulted in higher apoptosis rate of thymocytes(P<0.01).On the contrary,Ber improved the thymus atrophy(P<0.01),decreased cell death rate(P<0.05),reformed the MCAO/R-induced cell height(P<0.01) and average rough(P<0.05),reversed the higher apoptosis rate(P<0.05). Conclusion:Ber can significantly protect the MCAO/R injury by inhibiting thymocytes apoptosis.

Objective To study the expression of leukemic stem cell associated membrane antigens in acute leukemia cells with different subtypes.Methods Leukemic stem cell associated membrane antigens CD96,CD90,CD123 and CD71 were detected with flow cytometry in 50 acute leukemia patients with different subtypes including acute myeloblast leukemia without cell maturation(M1),acute myeloblast leukemia with cell maturation(M2),acute promyelocytic leukemia(M3),acute myelomonocytic leukemia(AMML) and B-acute lymphoblastic leukemia(B-ALL).Results The positive rate of CD96 expression in M3(90.00%) was significantly higher than that in M2(18.18%) and B-ALL(20.00%)(P<0.05).The up-regulation of CD123 was identified in all acute leukemia,and there was no significance difference in the subtypes(P>0.05).The positive rate of CD71 expression in four subtypes of acute myeloid leukemia(M1,M2,M3 and M4) was 80.00%,72.73%,90.00% and 100.00% respectively,all of which were significantly higher than those in B-ALL(20%)(P<0.05).There was no significant difference in CD90 expression between B-ALL(13.33%) and acute myeloid leukemia(P>0.05).Conclusion CD96 may become a marker for acute myeloid leukemia and its high expression might contribute to the overgrowth of acute myeloid leukemia cells.CD71 also may become a marker to distinguish acute myeloid leukemia from acute lymphoblastic leukemia for its higher expression in acute myeloid leukemia.

大量研究证实,子痫前期孕妇存在系统性的高氧化应激状态及炎症性免疫活化[1-2].研究发现,子痫前期孕妇血清中存在高水平的氧化应激产物H2O2,其可能来源于氧化应激性胎盘组织及外周大量活化的中性粒细胞[3].血管内皮细胞损伤和功能紊乱被认为是子痫前期疾病进展中的关键环节,而氧化应激和免疫细胞活化可能是引发内皮系统损伤的两个主要因素[4-5].但是,关于子痫前期氧化应激和免疫细胞活化之间的关系至今尚不明确.本研究旨在探讨子痫前期患者血清中H2O2在中性粒细胞及T淋巴细胞活化过程中的作用.

Objective To explore the potential mechanism on CD4+T cell loss in HIV and the regulation of CD4+T apoptosis by chuankezhi(CKZ)through the deep research of the impacts of HIVp on CD4+T apoptosis.Methods AT-2 was applied for the inactivation of HIV-1ⅢB viral granules.ELISA was used to detect the content of p24 antigen.HIVp was added into PBMCs so as to enable the terminal concentration of p24 antigen as 1ng·mL-1.CKZ was supplemented in corresponding groups so as to enable its terminal concentration as 40 μL·mL-1(v/v).48 h later,the fluorescence labeling Annexin V staining technique combined with flow cytometry(FCM)was adopted to evaluate the apoptosis rate of CD4+T cell.The immune fluorescent antibody staining technique combined with FCM was used to detect the expressions of CD95 and DR5 in CD4+T cell.The intracellular immune fluorescent antibody staining technique and molecular probe dyeing technique as well as FCM were combined together to detect Apo2.7 in CD4+7 cell and the level of mitochondrial membrane potential(△ψm).Results Compared with control group,HIVp induced an apparent CD4+T apoptosis(P0.01).CKZ could effectively inhibit CD4+T apoptosis induced by HIVp(P0.01).Conclusion HIVp deletes CD4+T cell via exogenous apoptosis and endogenous apoptosis and results in immune deficiency.CKZ can protect CD4+T and is expected to be developed as an aided medicine for the treatment of AIDS.

To explore the potential immunomodulatory effects and related mechanisms of ginkgolide B(GB),a known potent antagonist of platelet-activating factor receptor,we investigated the behaviors of T lymphocytes,including activation,proliferation and apoptosis.T lymphocytes were prepared from murine lymph nodes,and then treated with different concentrations of GB before cultivation.Activation and proliferation of T cells were induced by polyclonal activator concanavalin(Con A).Fluorescence conjugated monoclonal antibodies and flow cytometry were used to detect the expression of CD3/CD69 and CD3/CD25;CFDA-SE labeling and flow cytometry were used to trace the proliferation of T lymphocytes and an MTT assay was taken to re-prove.Apoptosis of T cells were induced by dexamethasone(Dex),while [DiOC6(3)/PI] staining and flow cytometry were used to distinguish apoptotic,dead and living cell populations.In a dose-dependent manner,GB(5,10,and 20 μmol/L) significantly suppressed the expression of CD69 at 6th h and CD25 at 24th h,as well as inhibited cell proliferation at 48th h after Con A stimulation.To some extent,GB also exhibited protective effect on T lymphocytes from Dex-induced apoptosis.According to these interesting effects of GB on T lymphocytes behaving and functioning,it's quite reasonable to do further studies of GB as a nature occurring immunomodulator candidate.

Objective:To explore the effects of ovariectomy(OVX)and estrogen replace treatment on total cholesterol,LDL,HDL,triglycerides,serum leptin and resist levels.Methods:Female SD rats(12 weeks)were divided into three groups: control Sham,OVX and OVX treated with estrogen(OVX +E2)(n=7,each group).10 days post operating,rats had been treated with estradiol benzoate(0.2 mg ip per day)(OVX + E2)and vehicle(Sham and OVX rats)for 30 days respectively.Total cholesterol,LDL,HDL,triglycerides were analyzed by chemistry analyzer,and ELISA kits were employed to analyze serum leptin and resistin levels.Results:Body mass was increased by OVX and significantly decreased by estrogen treatment.Total cholesterol and LDL level were upregulated after OVX.Estrogen treatment increase triglyceride level,while decreased total cholesterol and LDL level of OVX rats.No affect was found in serum leptin and resistin level of OVX or estrogen treatment groups.Conclusion:OVX led to body mass increase and lipid metabolism disturbance.Treated with E2,the body mass of the ovariectomized rats were decreased and the disturbance of lipid metabolism was partially improved.OVX and estrogen replacement can not affect serum leptin and resistin levels.

This study is designed to investigate the effects of ginsenoside Rg1 on murine peritoneal macrophages in vitro.The single cell suspension of murine peritoneal macrophages was prepared under sterile condition.After pre-incubated by Rg1 for 4 hours,the cells were stimulated with LPS at a final concentration of 10 μg/ml for 24 hours,then 1 μm diameter of the Yellow-Green Beads(1×1010/L) was added and the phagocytosis ability of macrophages was detected by flow cytometry(FCM).At the same time,the amount of NO produced by macrophages was detected by Griess kit,the ROS production by macrophages was assayed by H2DCFDA staining,the intracellular calcium concentration in macrophages was deteced by Fluo-4/AM staining.SytoxR Green plus Fluorescence Microplate Rader were used to detect the cells survive condition.The results showed Rg1 could inhibit the phagocytosis ability of macrophage stimulated with or without LPS.It also indicated that Rg1 could inhibit the production of NO and ROS both in the presence and absence of LPS.In addition,Rg1 could reduce the apoptosis of peritoneal macrophages induced by ION.Furthermore,Rg1 could inhibit the cell apoptosis induced by CHX and CTX.All these prompt Rg1 has an significant anti-inflammatory effects on macrophages,and can reduce the apoptosis induced by different stimuli,which provides a basis for the further development of Rg1 as an immune therapy drug.

To delineate the effects of ovariectomy(OVX) and genistein treatment on the levels of glucose,insulin,total cholesterol,LDL,HDL,triglycerides,serum leptin and resistin,female SD rats(12-week old) were divided into three groups,control(Sham),OVX and OVX treated with genistein(OVX+Gen)(n=7,each group).After operation for 10 days,rats were treated with genistein(ip,0.2 mg per day)(OVX+Gen) and vehicle(Sham and OVX rats) for 30 days.The pathological conditions of the uterus,and the levels of glucose,total cholesterol,LDL,HDL,triglycerides,serum leptin and resistin were analyzed.The results indicated that OVX upregulated the levels of total cholesterol,LDL and HDL,but showed no effect on the levels of insulin,blood glucose,triglyceride,serum leptin and resistin.Although the treatment with genistein did not change the levels of insulin,blood glucose,total cholesterol,triglyceride,LDL,HDL,serum leptin and resistin,it stimulated the proliferation of endometrial epithelial cells.The results suggest that genistein could promote the proliferation of endometrial epithelial cells,but show no effects of on the glucose and lipid metabolism,and the levels of serum leptin and resistin in ovariectomized female rats.