Expression of Nuclear Factor κB Activity in Peripheral Blood Mononuclear Cell in Elderly Patients With Early Type 2 Diabetic Nephropathy and Its Related Factors

目的 观察老年糖尿病肾病早期患者外周血单个核细胞中核因子-κB(NF-κB)p65磷酸化活化水平、血清炎症因子超敏C反应蛋白(hs-CRP)、肿瘤坏死因子α(TNF-α)、白介素6(IL-6)、白介素1β(IL-1β)水平,探讨NF-κB p65的磷酸化水平与胰岛素抵抗(HOMA-IR)、尿白蛋白排泄率(UAER)、糖脂代谢等因素的关系.方法 选择老年2型糖尿病肾病早期患者(DN组)66例及老年健康体检者对照组(NC组)30例为研究对象,测定外周静脉血NF-κB p65的磷酸化水平,血清炎症因子(hs-CRP、TNF-α、IL-6、IL-1β)水平,生化指标:空腹血糖(FBG)、餐后2 h血糖(PBG)、糖化血红蛋白(HbA1c)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、空腹胰岛素(FINS),测量身高、体重、血压,计算HOMA-IR、UAER.结果 DN组外周血NF-κB p65水平和血清炎症因子hs-CRP、TNF-α、IL-6、IL-1β水平比NC组升高(P＜0.05).相关分析显示,NF-κB与FBG、HbA1c、HOMA-IR、UAER呈正相关关系(r=0.920、0.953、0.911、0.859,P＜0.01).结论 老年糖尿病肾病早期患者外周血NF-κB表达水平升高,其表达水平与血糖控制水平、胰岛素抵抗、尿白蛋白排泄率相关.     

Dynamic Expression of Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor in Rat Model of Pulmonary Emphysema Induced by Smoke Exposure

In order to explore the roles of tumor necrosis factor-α(TNF-α) and vascular endothelial growth factor(VEGF) in the pathogenesis of pulmonary emphysema,male Wistar rats were randomized into group A1,group A2.5 and group A4,each with smoke exposure for 1 month,2.5 months or 4 months,respectively.Group B1,group B2.5 and group B4 were used as non smoking controls at corresponding time points.TNF-α in bronchoalveolar lavage fluid(BALF) and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either.Lung slices were stained with hematoxylin and eosin(HE).Results showed that in animal with smoke exposure the mean linear interceptor(Lm),an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually,on contrary,the expression of VEGF in lung tissue decreased(P<0.05).This phenomenon was not obvious in animals without smoke exposure.Lm was negatively correlated to the VEGF expression(γ=-0.81,P<0.01) and positively correlated to TNF-α concentration(γ = 0.52,P<0.004),which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α.It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.     

Compound Tufuling Granules (复方土茯苓颗粒) Regulate Glucose Transporter 9 Expression in Kidney to Influence Serum Uric Acid Level in Hyperuricemia Mice

Objective:To explore the effect of Compound Tufuling Granules(复方土茯苓颗粒,CTG) on regulating glucose transporter 9(GLUT9) expression in the kidney to influence the uric acid excretion by the kidney and serum uric acid(SUA) level in hyperuricemia mice.Methods:Sixty Kunming male mice were randomly divided into the control group,model group,benzbromarone group,and CTG high-,middle- and lowdose groups.The yeast extract and uricase inhibition method were used to build hyperuricemia model,and the corresponding drugs were administrated on the 7th day.On the 21 st day the 24-h urine was collected,on the 22 nd day the blood was collected,the SUA level was detected by uricase colorimetry,and the mRNA and protein expressions of GLUT9 were detected by quantitative real-time polymerase chain reaction and Western blot,respectively.Results:Compared with the model group,the levels of SUA and the mRNA and protein expressions of GLUT9 were significantly decreased,and the fraction excretion of uric acid(FEUA) was significantly increased in the CTG groups and benzbromarone group(all P0.05).There was no significant difference in the above indicators between the CTG high-dose group and benzbromarone group(P0.05).SUA is positively related to the GLUT9 mRNA and protein expressions in the kidney(P0.05 or P0.01).Conclusions:CTG can significantly reduce the SUA and increase the FEUA.In addition,CTG can effectively inhibit the mRNA and protein expressions of GLUT9 in the kidney of hyperuricemia mice to inhibit the uric acid re-absorption,promote uric acid excretion and reduce SUA.     

Effects on the Tumor Specific Growth Factor and Tumor Necrosis Factor α in Rats' Precancerous Lesion of Primary Hepatocellular Carcinoma by Direct Moxibustion at Ganshu(BL 18) Acupoint

Objective: To investigate the effect of direct moxibustion at Ganshu(BL18) on the serum concentrations of tumor specific growth factor(TSGF) and tumor necrosis factor α(TNF-α) in a rat model with precancerous lesion of primary hepatocellular carcinoma(HCC), so as to explore the mechanism of moxibustion underlying improvement of HCC. Methods: Sixty male Wistar rats were randomly divided into control group(n=10), model group(n=20), prevention group 1(n=15) and prevention group 2(n=15). The normal rats were injected with physiological saline as blank control. At the same time, the rats of other three groups were injected with diethylnitrosamine to establish the HCC model. Direct moxibustion with grain-sized moxa was applied to bilateral Ganshu acupoint of the rats in the prevention group 1(1 treatment course, 20 days) and prevention group 2(2 treatment courses, 40 days), 5 doses for each acupoint, 0.5 mg/dose, once every other day. At each time point(before model establishment, the end of 1st course prevention, the end of 2nd course prevention and the end of model establishment), serum levels of TSGF and TNF-α were detected using enzyme-linked immunosorbent assay. Results: Compared with the control group, there was a remarkably increase of serum TSGF and TNF-α contents in the model group at the end of the experiment(P0.05). At the end of the 1st course of direct moxibustion, the contents of serum TSGF and TNF-α of rats in the prevention group 1 were significantly increased compared with that of the model group(P0.05). At the end of the 2nd course of direct moxibustion, serum TSGF and TNF-α levels of rats in the model group were higher than the normal group with significantly difference(P0.05), and the levels of TSGF and TNF-α in the prevention group 2 were significantly reduced in comparison with the model group(P0.05). Conclusion: It was possible that direct moxibustion could inhibit precancerous lesion and postpone hepatocarcinogenesis, and the therapeutic effect of two courses were better than one course.     

Effect of Wenhua Juanbi Recipe (温化蠲痹方) on Expression of Receptor Activator of Nuclear Factor Kappa B Ligand, Osteoprotegerin, and Tumor Necrosis Factor Receptor Superfamily Member 14 in Rats with Collagen-Induced Arthritis

Objective: To study the effect of Wenhua Juanbi Recipe(温化蠲痹方, WJR) on expression of receptor activator of nuclear factor kappa B ligand(RANKL), osteoprotegerin(OPG), and tumor necrosis factor receptor superfamily member 14(TNFRSF14, also known as LIGHT) in rats with collagen-induced arthritis(CIA). Methods: CIA rats were generated by subcutaneous injection of bovine collagen type-Ⅱ at the tail base. Sixty CIA rats were randomly assigned(10 animals/group) to: model, methotrexate(MTX)-treated(0.78 mg/kg body weight), and WJR-treated(22.9 g/kg) groups. Healthy normal rats(n=10) were used as the normal control. Treatments or saline were administered once daily by oral gavage. Rats were sacrificed at day 28 post-treatment and knee synovium and peripheral blood serum were collected. Toe swelling degree and expression of RANKL, OPG, and LIGHT were determined by Western blot and immunohistochemistry. Results: Compared with the normal group, toe swelling degree was significantly increased in the model group(P0.01). After treatment, toe swelling degree decreased significantly in the WJR and MTX groups compared with the model group(P0.01). Compared with the normal group, expression of RANKL and LIGHT were significantly increased and OPG significantly decreased in peripheral blood and synovium of the model group(P0.01). Conversely, RANKL and LIGHT expression were significantly reduced and OPG increased in the WJR and MTX groups compared with the model group(P0.01). No statistically significant difference existed between WJR and MTX groups. Conclusion: WJR likely acts by reducing RANKL expression and increasing OPG expression, thus inhibiting RANKL/RANK interaction and reducing LIGHT expression, thereby inhibiting osteoclast formation/activation to block bone erosion.     

Effects of Curcumin on Pain Threshold and on the Expression of Nuclear Factor κB and CX3C Receptor 1 after Sciatic Nerve Chronic Constrictive Injury in Rats

Objective：To investigate the effects of curcumin on pain threshold and the expressions of nuclear factorκB（NF-κB）and CX3C chemokine receptor 1（CX3CR1）in spinal cord and dorsal root ganglion（DRG）of the rats with sciatic nerve chronic constrictive injury.Methods：One hundred and twenty male Sprague Dawley rats,weighing 220-250 g,were randomly divided into 4 groups.Sham surgery（sham）group：the sciatic nerves of rats were only made apart but not ligated;chronic constrictive injury（CCI）group：the sciatic nerves of rats were only ligated without any drug treatment;curcumin treated injury（Cur）model group：the rats were administrated with curcumin 100 mg/（kg·d）by intraperitoneal injection for 14 days after CCI;solvent control（SC）group：the rats were administrated with the solvent at the same dose for 14 days after CCI.Thermal withdrawal latency（TWL）and mechanical withdrawal threshold（MWT）of rats were respectively measured on pre-operative day 2 and postoperative day 1,3,5,7,10 and 14.The lumbar segment L4-5 of the spinal cord and the L4,L5 DRG was removed at post-operative day 3,7 and 14.The change of nuclear factorκB（NF-κB）p65 expression was detected by Western blotting while the expression of CX3CR1 was determined by immunohistochemical staining.Results：Compared with the sham group,the TWL and MWT of rats in the CCI group were significantly decreased on each post-operative day（P〈0.01）,which reached a nadir on the 3rd day after CCI,and the expressions of NF-κB p65and CX3CR1 were markedly increased in spinal cord dorsal horn and DRG.In the Cur group,the TWL of rats were significantly increased than those in the CCI group on post-operative day 7,10 and 14（P〈0.05）and MWT increased than those in the CCI group on post-operative day 10 and 14（P〈0.05）.In addition,the administration of curcumin significantly decreased the positive expressions of NF-κB p65 and CX3CR1 in spinal cord and DRG（P〈0.05）.Conclusion：Our study suggests that curcumin cou     

Protective Effect of Ganshuang Granules(肝爽颗粒)on Liver Cirrhosis by Suppressing Regulatory T Cells in Mouse Model

Objective: To investigate the potential antifibrotic mechanisms of Chinese medicine Ganshuang Granules(肝爽颗粒, GSG) and to provide clinical therapeutic evidence of its effects. Methods: A cirrhotic mouse model was established by intraperitoneally injecting a mixture of CCl_4(40%) and oil(60%) at 0.2 mL per 100 g of body weight twice a week for 12 weeks. After 12-week modeling, GSG was intragastric administrated to the mice for 2 weeks, and the mice were divided into low-, medium-and high-dose groups at doses of 1, 2 and 4 g/(kg·day), respectively. Liver morphology changes were observed using Masson's trichrome staining and B-ultrasound. The levels of alanine aminotransferase(ALT), aspartate aminotransferase(AST) and hyaluronic acid(HA) in serum were detected using an automatic biochemistry analyzer. The expressions of desmin, smooth muscle actin(SMA) and Foxp3 in liver were detected by immunofluorescence. The regulatory T cell(Treg) frequency was determined through flow cytometry analysis. Collagen-Ⅰ, SMA, IL-6, tumor necrosis factor α(TNF-α), interleukin(IL)-1β and transforming growth factor β1(TGF-β1) expression levels were measured using quantitative polymerase chain reaction(qPCR). Results: Masson's staining result showed fewer pseudolobule structures and fibrous connective tissue in the GSG-treatment groups than in the spontaneous recovery group. Ultrasonography showed that GSG treatment reduced the number of punctate hyperechoic lesions in mice cirrhotic livers. The serum ALT, AST, HA levels were significantly ameliorated by GSG treatment(ALT: F=8.104, P=0.000; AST: F=7.078, P=0.002; and HA: F=7.621, P=0.001). The expression levels of collagen-Ⅰ and SMA in the cirrhotic livers were also attenuated by GSG treatment(collagen-Ⅰ: F=3.938, P=0.011; SMA: F=4.115, P=0.009). Tregs, which were elevated in the fibrotic livers, were suppressed by GSG treatment(F=8.268, P=0.001). The expressions of IL-6, TNF-α and IL-1β increased, and TGF-β levels decreased in the cirrhotic livers after GSG treatment(IL-6: F=5.457, P=0.004; TNF-α: F=6.023, P=0.002; IL-1β: F=6.658, P=0.001; and TGF-β1: F=11.239, P=0.000). Conclusions: GSG promoted the resolution/regression of cirrhosis and restored liver functions in part by suppressing Treg cell differentiation, which may be mediated by hepatic stellate cells.     

Mechanism of Hewei Jiangni Capsule(和胃降逆胶囊)Regulating Proliferation and Apoptosis of Human Gastric Cancer AGS Cells Through PI3K/AKT Signaling Pathway

目的:探究和胃降逆胶囊对人胃癌AGS细胞增殖和凋亡的影响及其作用机制.方法:用不同药物剂量(3 g/kg、6 g/kg、12 g/kg)制备的和胃降逆胶囊含药血清分别干预人胃癌AGS细胞,分为和胃降逆胶囊含药血清低剂量组、中剂量组、高剂量组及空白组,分别干预AGS细胞24 h、48 h、72 h后,采用四甲基偶氮唑蓝(MTT)法检测细胞增殖情况,采用流式细胞仪检测细胞周期分布情况,蛋白质印迹法(Western blot)检测细胞相关蛋白磷酸化磷脂酰肌醇3-激酶(p-PI3K)、磷酸化蛋白激酶B(p-AKT)、促凋亡基因(Bax)、抑细胞凋亡蛋白(Bcl-2)、细胞周期蛋白D1 (Cyclin D1)和细胞周期蛋白依赖性抑制剂(p21)的表达情况;实时荧光定量聚合酶链式反应(RT-PCR)法检测细胞凋亡相关基因Bax、Bcl-2、Cyclin D1和p21 mRNA表达情况.结果:随着和胃降逆胶囊含药血清作用时间的延长,各药物组细胞活力逐渐降低,同剂量组24h、48 h、72 h比较差异有统计学意义(P＜0.05),48 h与72 h比较差异无统计学意义.在同一干预时间点,细胞活力随着药物血清浓度的增加而降低.各组含药血清处理AGS细胞48 h后,G0/G1期细胞比值与空白组比较,差异具有统计学意义(P＜0.05);和胃降逆胶囊可以下调AGS细胞中p-PI3K、p-AKT蛋白及抑制凋亡蛋白Bcl-2和Cyclin D1的表达(P＜0.05),上调AGS细胞中促凋亡蛋白Bax和p21的表达(P＜0.05);和胃降逆胶囊可以下调AGS细胞中抑制凋亡基因Bcl-2和Cyclin D1 mRNA的表达(P＜0.05),上调AGS细胞中促凋亡基因Bax和p21 mRNA的表达(P＜0.05),且呈现出浓度相关性.结论:和胃降逆胶囊通过抑制PI3K/AKT通路的活化,调控下游周期阻滞相关基因和凋亡相关基因的表达,进而抑制人胃癌AGS细胞增殖并促进AGS细胞凋亡.     

Effect of Combination of Bushen Jianpi Recipe (补肾健脾方) and Erythropoietin on Serum Tumor Necrosis Factor a in Patients with Anemia

Objective: To study the effect of treatment of renal anemia by combination of Bushen Jianpi Recipe (补贤健脾方, BJR, a Chinese experienced recipe for supplementing Shen and supporting Pi) and low dosage erythropoietin (EPO), and the influence of treatment on change of serum tumor necrosis factor α (TNF-α) so as to explore the possible mechanism of integrative Chinese and Western medicine (ICWM) in treating renal anemia. Methods: Patients with renal anemia were randomly divided into two groups, the ICWM group and the control group, supporting treatment such as dialysis, supplementing of ferrous, foliac acid and vitamin B12, was given to both groups. Additionally, to the ICWM group, 50 IU/kg of EPO subcutaneous injection for twice every week, and oral intake of BJR, one dose per day taken in two parts, were given, and to the control group, EPO alone, 50IU/kg by subcutaneous injecting, 3 times perweek, was given. The therapeutic course for two groups was 3 months. Blood levels of hemoglobin (Hb), hematoc     

Guizhi Decoction (桂枝汤) Inhibits Cholinergic Transdifferentiation by Regulating Imbalance of NGF and LIF in Salt-Sensitive Hypertensive Heart Failure Rats

Objective: To observe the imbalance of anatomical and functional innervation factors of sympathetic nerves, nerve growth factor(NGF) and leukemia inhibitory factor(LIF), in salt-sensitive hypertensive heart failure rats and to explore the effects of treatment with Guizhi Decoction(桂枝汤) on sympathetic remodeling by inhibiting cholinergic transdifferentiation. Methods: SS-13 BN and Dahl salt-sensitive(DS) rats were divided into 3 groups: SS-13 BN group(control group, n=9), DS group(model group, n=9) and GS group(Guizhi Decoction, n=9). After 10 weeks of a high-salt diet, the GS group rats were given Guizhi Decoction and other two groups were given saline at an equal volume as a vehicle. After 4 weeks' intragastric administration, rats were executed to detect the relevant indicators. Echocardiography and plasma n-terminal pro-B type natriuretic peptide(NT-proBNP) levels were used to assess cardiac function. Noradrenaline(NA) levels in the plasma and myocardium were detected to evaluate the sympathetic function. NGF and LIF expression were detected in the myocardium by Western blot or quantitative real-time PCR. Double immunofluorescence or Western blot was used to detect tyrosine hydroxylase(TH), choline acetyltransferase(CHAT) and growth associated protein 43(GAP43) in order to reflect anatomical and functional changes of sympathetic nerves. Results: DS group had anatomical and functional deterioration of sympathetic nerves in the decompensation period of heart failure compared with SS-13 BN group. Compared with the DS group, Guizhi Decoction significantly decreased the expression of LIF mRNA/protein(P0.01), increased the expression of NGF(P0.05 or P0.01), enhanced the levels of TH~+/GAP43~+ and TH~+/CHAT~+ positive nerve fibers(P0.01), and improved the protein expression of TH and GAP43 in left ventricle, but had no effect on CHAT(P0.05). Guizhi Decoction inhibited inflammatory infiltration and collagen deposition of myocardial injury, increased the content of myocardial NA(P0.05), reduced the plasma NA level(P0.01), improved cardiac function(P0.01), and improved weight and blood pressure to some extent(P0.05), compared with DS group. Conclusions: Guizhi Decoction could inhibit cholinergic transdifferentiation of sympathetic nerves, improve the anatomical and functional denervation of sympathetic nerves, and delay the progression of decompensated heart failure. The mechanism may be associated with the correction of the imbalance of NGF and LIF.     

Effects of Zuogui Pill(左归丸) and Yougui Pill(右归丸) on the Expression of Brain-Derived Neurotrophic Factor and Cyclic Adenosine Monophosphate/Protein Kinase A Signaling Transduction Pathways of Axonal Regeneration in Model Rats with Experimental Autoimm

Objective:To study the effects of Zuogui Pill(左归丸,ZGP)and Yougui Pill(右归丸,YGP)on the expressions of brain-derived neurotrophic factor(BDNF)and cyclic adenosine monophosphate(cAMP)/protein kinase A(PKA)signaling of axonal regeneration in the Lewis rats with experimental autoimmune encephalomyelitis(EAE),in order to explore the possible mechanism of ZGP and YGP on promoting axonal regeneration.Methods:The rats were randomly divided into normal control(NC),model(MO),prednisone acetate(PA),ZGP and YGP groups.The EAE model of rat was established by injecting antigen containing myelin basic protein(MBP)_(68-86).The brain and spinal cord were harvested on the 14th and 28th day postimmunization(PI),the protein and mRNA expression of BDNF and PKA in the brain and spinal cord of rats were detected by Western blot analysis and real-time quantitative polymerase chain reaction(PCR),and the cAMP levels were detected by using enzyme-immunoassay method.Results:(1)On the 28th day PI,the mRNA expression of BDNF in brain white matter and spinal cord of rats in ZGP and YGP groups were up-regulated,especially in YGP group(P0.05 or P0.01).(2)On the 14th day PI,the cAMP levels in brain white matters significantly increased in PA and YGP groups compared with MO group(P0.05 or P0.01),and the cAMP level in YGP group was higher than that in ZGP group(P0.05).The cAMP level in spinal cord also significantly increased in YGP group compared with MO,PA and ZGP groups,respectively(P0.01).(3)On the 14th day PI,the PKA expression in spinal cord of rats in ZGP group was significantly decreased compared with MO and YGP groups,respectively(P0.05).(4)On the 28th day PI,there was a positive correlation between cAMP and PKA expression in the brain white matter of YGP rats.Conclusions:The results suggest that ZGP and YGP may promote axonal regeneration by modulating cAMP/PKA signal transduction pathway,but the targets of molecular mechanism of ZGP may be different from those of YGP.     

Qushi Huayu Decoction (祛湿化瘀方) Inhibits Protein and Gene Expression of Cathepsin B in HepG2 Cells Induced by Free Fatty Acids

Objective: To study the experimental efficacy of Qushi Huayu Decoction (祛湿化瘀方,QHD) on protein and gene expression of cathepsin B (ctsb) in HepG2 cells induced by free fatty acids (FFAs).Methods: The model of HepG2 steatosis and tumor necrosis factor-α (TNF-α) secretion was induced by long-chain FFAs.HepG2 cells were divided into 4 groups: control group (group C),model group (group M),low-dose QHD group (group L) and high-dose QHD group (group H ).Long-chain FFAs were added to groups M,L and H.The 10% blank-control serum was added to group C and M,while 5% and 10% QHD-containing sera were added to group L and H,respectively.The levels of serum TNF-α and cellular triglyceride (TG) were detected.Cellular p-IκB and ctsb expression were detected using Western blot and PCR.The expression and distribution of ctsb were observed by immunofluorescence.Results: After incubating with FFA for 24 h,TG deposition in HepG2,TNF-α content in cell supernatant,the protein expression of cellular ctsb and P-IκB,as well as mRNA expression of ctsb increased markedly in group M compared with group C (P0.05,P0.01).Compared with group M,TG deposition,the expression of cellular ctsb,P-IκB and ctsb mRNA in groups L and H,as well as TNF-α content in group H,decreased significantly (P0.05).Cell immunochemical fluorescence studies showed that ctsb was released from lysosomes and distributed in the cytoplasm extensively and diffusedly after being stimulated with FFA.In this study,these above-mentioned changes were inhibited markedly in groups L and H.Conclusion: QHD might have a direct inhibitory effect on the ctsb target in the FFA-ctsb-TNFα pathway of hepatic lipotoxicity.     

Xuefu Zhuyu Oral Liquid (血府逐瘀口服液) Prevents Apoptosis of Ischemic Myocardium Cells in Rats by Regulating SIRT1 and Its Pathway-Related Genes

Objective: To observe the changes of ischemic myocardial cells apoptosis in rats following intervention with Xuefu Zhuyu Oral Liquid(血府逐瘀口服液, XFZY), as well as changes of protein expression of silent information regulator 1(SIRT1) and SIRT1 pathway-related genes. Methods: H9c2 rat myocardial cells were divided into 6 groups: control group, oxygen glucose deprivation(OGD) group, SIRT1 siRNA group, OGD+SIRT1 siRNA group, OGD+XFZY group, and OGD+SIRT1 siRNA+XFZY group. Quantitative fluorescent polymerase chain reaction(PCR) and Western blot were used to detect the concentration variations of SIRT1 and its pathway-related genes and corresponding protein expression after XFZY intervention and SIRT1 transfection. Results: Compared with the control group, the m RNA and protein expressions of SIRT1 were decreased obviously, while the mRNA and protein levels of P53, forkhead box protein O1(FoxO1), FoxO3, FoxO4 and nuclear factor kappa B(NF-κB) were increased in the OGD group, SIRT1 siRNA group, and OGD+SIRT1 siRNA group(P0.01). Compared with the OGD group and OGD+SIRT1 siRNA group, the treatment of XFZY inhibited the decline in SIRT1 mRNA and protein expressions(P0.01), and down-regulated the mRNA and protein levels of P53, FoxO1, FoxO3, FoxO4 and NF-κB, respectively(P0.05 or P0.01). Conclusion: XFZY could prevent myocardial cells apoptosis probably by increasing the mRNA and protein expressions of SIRT1 and inhibiting the m RNA and protein expressions of P53, NF-κB, FoxO1, FoxO3 and FoxO4.     

Bushen Qiangji Granule(补肾强脊颗粒)Medicated Serum Inhibits Osteogenic Differentiation of Fibroblasts in Ankylosing Spondylitis by Inhibiting the BMP/Smads Signal Pathway in vitro

Objective: To explore the mechanism of Bushen Qiangji Granule(补肾强脊颗粒, BSQJ) in restraining the osteogenic differentiation of ankylosing spondylitis(AS) fibroblasts. Methods: Hip joint capsules were obtained from AS patients(n=10) receiving total hip replacement and healthy hip joint capsules from patients with hip fracture(n=10) receiving surgery as a control. Finite fibroblast lines were established from these tissue samples to observe the effect of BSQJ on suppressing osteogenic differentiation of fibroblasts. The expression of osteogenic marker gene corebinding factor a1(Cbfa1) and Smad family proteins were examined by Western blot and real-time quantitative polymerase chain reaction(q PCR). Results: The m RNA expression level of Cbfa1 was significantly higher in AS fibroblasts than that in normal fibroblasts and the expression of p Smad1, p Smad5, Smad4 and Cbfa1 in AS fibroblasts was also higher, demonstrating the activation of the BMP/Smads signal pathway in AS fibroblasts. BSQJ-medicated serum not only restrained the m RNA and protein expression levels of Cbfa1 and inhibited protein expression level of Smad4 but also decreased the expression quantities of p Smad1 and p Smad5. Conclusions: BSQJ can inhibit osteogenic differentiation of AS fibroblasts in vitro by suppressing the activation of the BMP/Smads signal pathway. This may be the important molecular mechanism of BSQJ in regulating AS ossification.     

Fuzheng Yiliu Granule (扶正抑瘤颗粒) inhibits the growth of hepatocellular cancer by regulating immune function and inducing apoptosis in vivo and in vitro

Objective  

To study the inhibitory effect of Fuzheng Yiliu Granule (扶正抑瘤颗粒, FYG) on hepatocellular cancer (HCC) and investigate the mechanism mediating its bioactivity.