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Electroacupuncture improves myocardial fibrosis in heart failure rats by attenuating ECM collagen deposition through modulation of TGF-β1/Smads signaling pathway
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作者 Wen-Hui Wang Qian-Lan Zeng +3 位作者 Jiao-Jiao Zhang Hao-Sheng Wu Sheng-Bing Wu Mei-Qi Zhou 《Traditional Medicine Research》 2024年第8期1-10,共10页
Background: To explore the effects of electroacupuncture on cardiac function and myocardial fibrosis in rat models of heart failure, and to elucidate the underlying mechanism of electroacupuncture in heart failure tre... Background: To explore the effects of electroacupuncture on cardiac function and myocardial fibrosis in rat models of heart failure, and to elucidate the underlying mechanism of electroacupuncture in heart failure treatment. Methods: Healthy male Sprague-Dawley rats were allocated into three groups: Sham group, Model group, and electroacupuncture (Model + EA) group, with each group comprising 8 rats. The model underwent a procedure involving the ligation of the left anterior descending coronary artery to induce a model of heart failure. The Model + EA group was used for 7 consecutive days for electroacupuncture of bilateral Shenmen (HT7) and Tongli (HT5), once a day for 30 min each time. Left ventricular parameters in rats were assessed using a small-animal ultrasound machine to analyze changes in left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular ejection fraction, and left ventricular fractional shortening. Serum interleukin-1β (IL-1β), cardiac troponin (cTn), and N-terminal brain natriuretic peptide precursor levels were measured using ELISA. Histopathological changes in rat myocardium were observed through HE staining, while collagen deposition in rat myocardial tissue was assessed using the Masson staining method. Picro sirius red staining, immunohistochemical staining, and RT-qPCR were utilized to distinguish between the various types of collagen deposition. The expression level of TGF-β1 and SMAD2/3/4/7 mRNA in rat myocardial tissues was determined using RT-qPCR. Additionally, western blot analysis was conducted to assess the protein expression levels of TGF-β1, SMAD3/7, and p-SMAD3 in rat myocardial tissues. Results: Compared with the Sham group, the left ventricular ejection fraction and left ventricular fractional shortening values of the Model group were significantly decreased (P < 0.01);the left ventricular end-diastolic volume and left ventricular end-systolic volume values were remarkably increased (P < 0.01);serum N-terminal brain natriuretic peptide precursor content was increased (P < 0.01);serum IL-1β and cTn levels were increased (P < 0.01);myocardial collagen volume fraction were increased (P < 0.01);and those of the expression of TGF-β1 and SMAD2/3/4 mRNA was increased (P < 0.01);the expression of SMAD7 mRNA was decreased (P < 0.01);the protein expression levels of TGF-β1, SMAD3, and p-Smad3 were increased (P < 0.01);the protein expression level of SMAD7 was decreased (P < 0.01) in the Model group. Compared to the Model group, the expression levels of the proteins TGF-β1, SMAD3, and p-Smad3 in myocardial tissue were found to be decreased (P < 0.01), and the expression level of the protein SMAD7 was found to be increased (P < 0.01) in the Model + EA group;the collagen volume fraction and deposition of type Ⅰ /Ⅲ collagen were decreased (P < 0.01) in the Model + EA group. Conclusion: Electroacupuncture alleviates myocardial fibrosis in rats with heart failure, and this effect is likely due to attributed to the modulation of the TGF-β1/Smads signaling pathway, which helps reduce collagen deposition in the extracellular matrix. 展开更多
关键词 heart failure ELECTROACUPUNCTURE heart meridian of Hand-Shaoyin collagen deposition tgf1/smads signaling pathway myocardial fibrosis
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MiR-146a-5p targeting SMAD4 and TRAF6 inhibits adipogenensis through TGF-β and AKT/mTORC1 signal pathways in porcine intramuscular preadipocytes 被引量:13
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作者 Que Zhang Rui Cai +2 位作者 Guorong Tang Wanrong Zhang Weijun Pang 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2021年第1期220-235,共16页
Background: Intramuscular fat(IMF) content is a vital parameter for assessing pork quality. Increasing evidence has shown that microRNAs(miRNAs) play an important role in regulating porcine IMF deposition. Here, a nov... Background: Intramuscular fat(IMF) content is a vital parameter for assessing pork quality. Increasing evidence has shown that microRNAs(miRNAs) play an important role in regulating porcine IMF deposition. Here, a novel miRNA implicated in porcine IMF adipogenesis was found, and its effect and regulatory mechanism were further explored with respect to intramuscular preadipocyte proliferation and differentiation.Results: By porcine adipose tissue miRNA sequencing analysis, we found that miR-146a-5p is a potential regulator of porcine IMF adipogenesis. Further studies showed that miR-146a-5p mimics inhibited porcine intramuscular preadipocyte proliferation and differentiation, while the miR-146a-5p inhibitor promoted cell proliferation and adipogenic differentiation. Mechanistically, miR-146a-5p suppressed cell proliferation by directly targeting SMAD family member 4(SMAD4) to attenuate TGF-β signaling. Moreover, miR-146a-5p inhibited the differentiation of intramuscular preadipocytes by targeting TNF receptor-associated factor 6(TRAF6) to weaken the AKT/mTORC1 signaling downstream of the TRAF6 pathway.Conclusions: MiR-146a-5p targets SMAD4 and TRAF6 to inhibit porcine intramuscular adipogenesis by attenuating TGF-β and AKT/mTORC1 signaling, respectively. These findings provide a novel miRNA biomarker for regulating intramuscular adipogenesis to promote pork quality. 展开更多
关键词 Adipogenesis AKT/mTORC1 signal pathway MiR-146a-5p Porcine intramuscular fat smad4 tgfsignal pathway TRAF6
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Berberine Attenuates Cigarette Smoke Extract-induced Airway Inflammation in Mice:Involvement of TGF-β1/Smads Signaling Pathway 被引量:6
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作者 Wen WANG Gan ZHA +3 位作者 Jin-jing ZOU Xun WANG Chun-nian LI Xiao-jun WU 《Current Medical Science》 SCIE CAS 2019年第5期748-753,共6页
Although several studies confirmed that berberine may attenuate airway inflammation in mice with chronic obstructive pulmonary disease(COPD),its underlying mechanisms were not clear until now.We aimed to establish an ... Although several studies confirmed that berberine may attenuate airway inflammation in mice with chronic obstructive pulmonary disease(COPD),its underlying mechanisms were not clear until now.We aimed to establish an experiment mouse model for COPD and to investigate the effects of berberine on airway inflammation and its possible mechanism in COPD model mice induced by cigarette smoke extract(CSE).Twenty SPF C57BL/6 mice were randomly divided into PBS control group,COPD model group,low-dose berberine group and high-dose berberine group,5 mice in each group.The neutrophils and macrophages were examined by Wright's staining.The levels of inflammatory cytokines TNF-α and IL-6 in bronchoalveolar lavage fluid(BALF)were detennined by enzyme-linked immunosorbent assay.The expression levels of TGF-β1,Smad2 and Smad3 mRNA and proteins in lung tissues were respectively detected by quantitative real-time polymerase chain reaction and Western blotting.It was found that CSE increased the number of inflammation cells in BALF,elevated lung inflammation scores,and enhanced the TGF-β1/Smads signaling activity in mice.High-dose berberine restrained the alterations in the COPD mice induced by CSE.It was concluded that high-dose berberine ameliorated CSE-induced airway inflammation in COPD mice.TGF-β1/Smads signaling pathway might be involved in the mechanism.These findings suggested a therapeutic potential of high-dose berberine on the CSE-induced airway inflammation. 展开更多
关键词 BERBERINE CIGARETTE SMOKE extract chronic OBSTRUCTIVE pulmonary disease tgf1/smads signaling pathway
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Calcitriol attenuates liver fibrosis through hepatitis C virus nonstructural protein 3-transactivated protein 1-mediated TGF β1/Smad3 and NF-κB signaling pathways 被引量:1
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作者 Liu Shi Li Zhou +13 位作者 Ming Han Yu Zhang Yang Zhang Xiao-Xue Yuan Hong-Ping Lu Yun Wang Xue-Liang Yang Chen Liu Jun Wang Pu Liang Shun-Ai Liu Xiao-Jing Liu Jun Cheng Shu-Mei Lin 《World Journal of Gastroenterology》 SCIE CAS 2023年第18期2798-2817,共20页
BACKGROUND Hepatic fibrosis is a serious condition,and the development of hepatic fibrosis can lead to a series of complications.However,the pathogenesis of hepatic fibrosis remains unclear,and effective therapy optio... BACKGROUND Hepatic fibrosis is a serious condition,and the development of hepatic fibrosis can lead to a series of complications.However,the pathogenesis of hepatic fibrosis remains unclear,and effective therapy options are still lacking.Our group identified hepatitis C virus nonstructural protein 3-transactivated protein 1(NS3TP1) by suppressive subtractive hybridization and bioinformatics analysis,but its role in diseases including hepatic fibrosis remains undefined.Therefore,additional studies on the function of NS3TP1 in hepatic fibrosis are urgently needed to provide new targets for treatment.AIM To elucidate the mechanism of NS3TP1 in hepatic fibrosis and the regulatory effects of calcitriol on NS3TP1.METHODS Twenty-four male C57BL/6 mice were randomized and separated into three groups,comprising the normal,fibrosis,and calcitriol treatment groups,and liver fibrosis was modeled by carbon tetrachloride(CCl4).To evaluate the level of hepatic fibrosis in every group,serological and pathological examinations of the liver were conducted.TGF-β1 was administered to boost the in vitro cultivation of LX-2 cells.NS3TP1,α-smooth muscle actin(α-SMA),collagen I,and collagen Ⅲ in every group were examined using a Western blot and real-time quantitative polymerase chain reaction.The activity of the transforming growth factor beta 1(TGFβ1)/Smad3 and NF-κB signaling pathways in each group of cells transfected with pcDNA-NS3TP1 or siRNA-NS3TP1 was detected.The statistical analysis of the data was performed using the Student’s t test.RESULTS NS3TP1 promoted the activation,proliferation,and differentiation of hepatic stellate cells(HSCs)and enhanced hepatic fibrosis via the TGFβ1/Smad3 and NF-κB signaling pathways,as evidenced by the presence of α-SMA,collagen I,collagen Ⅲ,p-smad3,and p-p65 in LX-2 cells,which were upregulated after NS3TP1 overexpression and downregulated after NS3TP1 interference.The proliferation of HSCs was lowered after NS3TP1 interference and elevated after NS3TP1 overexpression,as shown by the luciferase assay.NS3TP1 inhibited the apoptosis of HSCs.Moreover,both Smad3 and p65 could bind to NS3TP1,and p65 increased the promoter activity of NS3TP1,while NS3TP1 increased the promoter activity of TGFβ1 receptor I,as indicated by coimmunoprecipitation and luciferase assay results.Both in vivo and in vitro,treatment with calcitriol dramatically reduced the expression of NS3TP1.Calcitriol therapy-controlled HSCs activation,proliferation,and differentiation and substantially suppressed CCl4-induced hepatic fibrosis in mice.Furthermore,calcitriol modulated the activities of the above signaling pathways via downregulation of NS3TP1.CONCLUSION Our results suggest that calcitriol may be employed as an adjuvant therapy for hepatic fibrosis and that NS3TP1 is a unique,prospective therapeutic target in hepatic fibrosis. 展开更多
关键词 Nonstructural protein 3-transactivated protein 1 CALCITRIOL Liver fibrosis Hepatic stellate cells Mouse model tgfβ1/smad3 NF-κB signaling pathway
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基于TGF-β_(1)/Smads信号通路探讨大蒜素对2型糖尿病大鼠肾纤维化的影响
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作者 白敏 李晓翠 +2 位作者 靳世英 李慧 吴洁 《西部中医药》 2024年第3期5-9,共5页
目的:探讨大蒜素对2型糖尿病(type 2 diabetes mellitus,T2DM)大鼠肾纤维化和TGF-β_(1)/Smads信号通路的影响以及大蒜素对T2DM所致肾纤维化的作用机制。方法:将50只SD大鼠随机分为正常对照组、模型组和大蒜素低剂量组(5 mg/kg)、大蒜... 目的:探讨大蒜素对2型糖尿病(type 2 diabetes mellitus,T2DM)大鼠肾纤维化和TGF-β_(1)/Smads信号通路的影响以及大蒜素对T2DM所致肾纤维化的作用机制。方法:将50只SD大鼠随机分为正常对照组、模型组和大蒜素低剂量组(5 mg/kg)、大蒜素中剂量组(10 mg/kg)、大蒜素高剂量组(20 mg/kg),每组10只。正常对照组大鼠常规饲养,其余各组采用高糖高脂饲料喂养加腹腔注射链尿佐菌素的方法复制T2DM大鼠模型。造模完成后,大蒜素各剂量组大鼠腹腔注射相应剂量大蒜素溶液,正常对照组及模型组腹腔注射等剂量生理盐水,每天1次,共4周。干预4周后,测定各组大鼠空腹血糖水平,称量体质量;生化分析法测定24h尿蛋白(24 hour urine protein,24h UP)、血清尿素氮(blood urea nitrogen,BUN)、血清肌酐(serum creatinine,SCr)表达水平;苏木精-伊红染色法(hematoxylin-eosin staining,HE)进行肾组织病理学检查;Masson染色进行肾组织纤维化检查并计算胶原容积分数(collagen volume fraction,CVF);免疫组织化学(immunohistochemistry,IHC)法检测肾组织中转化生长因子β_(1)(transforming growth factor-β_(1),TGF-β_(1))、磷酸化Smad2(phospho-Smad2,p-Smad2)、p-Smad3蛋白表达以及Ⅰ型胶原蛋白(collagenⅠ,ColⅠ)和Ⅲ型胶原蛋白(collagenⅢ,ColⅢ)表达。结果:与正常对照组比较,模型组大鼠肾小球增大、系膜基质增厚、肾小管上皮细胞空泡变性、炎性细胞浸润,大鼠空腹血糖、24h UP、BUN、SCr、CVF、TGF-β_(1)、p-Smad2、p-Smad3、Col I、ColⅢ均升高,体质量下降;与模型组比较,大蒜素中、高剂量组大鼠空腹血糖水平降低、体质量升高(P<0.05),24h UP和血清BUN、SCr水平降低(P<0.01),病理学改变改善;与模型组比较,大蒜素低、中、高剂量组大鼠肾组织纤维化改善,肾组织CVF降低(P<0.01);与模型组比较,大蒜素中、高剂量组大鼠肾组织TGF-β_(1)、p-Smad2、p-Smad3、Col I、ColⅢ蛋白表达下调(P<0.01)。结论:大蒜素对T2DM大鼠肾纤维化具有抑制作用,其机制可能与大蒜素调控TGF-β_(1)/Smads信号通路进而抑制细胞外基质生成有关。 展开更多
关键词 2型糖尿病 肾纤维化 胶原蛋白 tgf-β_(1)/smads信号通路 大蒜素
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Cetirizine regulates scleroderma skin fibrosis in mice via the TGF-β1/Smad3 signaling pathway
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作者 Feng Jian Jing Qi +3 位作者 Xiao-Ying Yang Li-Na Yang Qi Zhang Xiang Li 《Journal of Hainan Medical University》 2020年第14期16-21,共6页
Objective:To investigate the effect of cetirizine on the fibrosis of skin tissue in systemic sclerosis(SSc)mice and its mechanism of action.Methods:Thirty-two BALB/C mice were randomly divided into a blank group,a mod... Objective:To investigate the effect of cetirizine on the fibrosis of skin tissue in systemic sclerosis(SSc)mice and its mechanism of action.Methods:Thirty-two BALB/C mice were randomly divided into a blank group,a model group,a cetirizine low-dose group,and a cetirizine high-dose group,with eight in each group.The blank group was injected with normal saline on the back,and the other three groups were injected with bleomycin on the back to prepare SSc mouse models.The mice were injected once a day for 28 consecutive days,while the normal group and the model group were given saline.The dose group was administrated intragastrically at 2 mg/kg and 5 mg/kg,respectively,for 28 consecutive days.Detect the thickness of the dermis by taking the skin tissue in the back injection area of each group.Hematoxylin-eosin staining(HE)and Masson staining.Sample hydrolysis method to detect hydroxyproline(HYP)content in skin tissue.Immunohistochemical detection ofα-smooth muscle actin(α-SMA)expression in skin tissues.Enzyme-linked immunosorbent assay(ELISA)to detect serum interleukin(IL-6,IL-10)and transforming growth factor(TGF-αand TGF-β1).Quantitative real-time PCR(qRT-PCR)was used to detect the expression levels of collagen type I(COL1A1),type III collagen(COL3A1),Smad homolog 3(Smad3),and TGF-β1 mRNA.Western blot was used to detect the expression levels of COL1A1,COL3A1 and p-Smad3.Results:Compared with the blank group,the dermis thickness and HYP content of the model group increased,the skin tissue lesions and fibrosis were more severe,theα-SMA positive expression intensity in the skin tissue was higher,and the serum IL-6,IL-10,TGF-α,TGF-β1 content increased,COL1A1,COL3A1,Smad3,TGF-β1 mRNA expression levels increased in skin tissues,COL1A1,COL3A1,p-Smad3 protein expression increased,the differences were statistically significant(P<0.05).Compared with the model group,the dermal thickness and HYP content of the low and high dose cetirizine groups were reduced,the degree of skin tissue lesions and fibrosis was improved,the expression ofα-SMA in skin tissues was weakened,the levels of IL-6,IL-10,TGF-α,TGF-β1 in serum were reduced,the expression levels of COL1A1,COL3A1,Smad3 and TGF-β1 in skin tissues were reduced,and the expression levels of COL1A1,COL3A1,and p-Smad3 proteins were reduced,the decrease in the high-dose group was more significant,and the differences were statistically significant(P<0.05).Conclusion:Cetirizine can improve the degree of fibrosis of skin tissue in SSc mice and reduce the immune inflammation response.The mechanism of action is related to the TGF-β1/Smad3 signaling pathway. 展开更多
关键词 SCLERODERMA CETIRIZINE Skin fibrosis tgf1/smad3 signaling pathway
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基于TGF-β_(1)/Smads信号通路的中药防治支气管哮喘研究进展 被引量:2
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作者 张智博 赵克明 《西部中医药》 2024年第1期95-99,共5页
基于TGF-β_(1)/Smads信号通路对支气管哮喘的影响及中药干预作用研究进展进行综述,指出转化生长因子β_(1)(transforming growth factor-β_(1),TGF-β_(1))对哮喘发病过程中气道炎症与气道重塑的病理基础发挥作用,TGF-β_(1)对气道炎... 基于TGF-β_(1)/Smads信号通路对支气管哮喘的影响及中药干预作用研究进展进行综述,指出转化生长因子β_(1)(transforming growth factor-β_(1),TGF-β_(1))对哮喘发病过程中气道炎症与气道重塑的病理基础发挥作用,TGF-β_(1)对气道炎症具有双重作用,既可通过刺激嗜酸性粒细胞促进气道炎症发生,又可通过刺激肥大细胞产生白细胞介素6,抑制气道炎症;此外,因TGF-β_(1)具有超强的致纤维化作用,可促进成纤维细胞生长,引起气道重塑,中药可通过调控TGF-β_(1)/Smads信号通路,从而干预哮喘发作,缓解哮喘临床症状。 展开更多
关键词 支气管哮喘 tgf-β_(1)/smads信号通路 中药 综述
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祛风扶阳汤对支气管哮喘大鼠TGF-β_(1)/Smad信号通路与Th17/Treg失衡的影响
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作者 范彩虹 张豪杰 姚梓平 《现代中西医结合杂志》 CAS 2024年第17期2364-2370,共7页
目的观察祛风扶阳汤对支气管哮喘大鼠气道炎症、气道重塑、转化生长因子-β_(1)(TGF-β_(1))/Smad信号通路及辅助性T细胞17(Th17)/调节性T细胞(Treg)失衡的影响,探究其作用及机制。方法将45只SD大鼠随机分为空白组、哮喘组、地塞米松组... 目的观察祛风扶阳汤对支气管哮喘大鼠气道炎症、气道重塑、转化生长因子-β_(1)(TGF-β_(1))/Smad信号通路及辅助性T细胞17(Th17)/调节性T细胞(Treg)失衡的影响,探究其作用及机制。方法将45只SD大鼠随机分为空白组、哮喘组、地塞米松组、祛风扶阳汤中剂量组、祛风扶阳汤高剂量组,每组9只。除空白组外,其余组大鼠均采用卵蛋白腹腔注射和雾化吸入方法建立支气管哮喘模型。建模成功后,地塞米松组给予地塞米松0.001 g/kg灌胃,祛风扶阳汤中、高剂量组分别给予祛风扶阳汤9.95 g/kg和19.9 g/kg灌胃,空白组和哮喘组灌胃等量生理盐水,均1次/d,连续灌胃4周。记录各组大鼠末次灌胃后咳嗽次数,HE染色观察肺组织病理形态,ELISA法检测肺泡灌洗液中白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、白细胞介素-17A(IL-17A)、TGF-β_(1)水平,Western blot法检测肺组织中TGF-β_(1)、α-平滑肌肌动蛋白(α-SMA)、Smad2/3、p-Smad2/3蛋白表达情况,流式细胞仪检测肺组织中IL-17A^(+)CD4^(+)、CD4^(+)CD25^(+)Foxp3^(+)Treg比例。结果与空白组比较,哮喘组大鼠咳嗽次数明显增加(P<0.05),肺泡灌洗液中IL-6、IL-17A、TGF-β_(1)水平和肺组织中TGF-β_(1)、α-SMA、p-Smad2/3蛋白相对表达量及IL-17A^(+)CD4^(+)比例均明显升高(P均<0.05),肺泡灌洗液中IL-10水平和肺组织中CD4^(+)CD25^(+)Foxp3^(+)Treg比例均明显降低(P均<0.05);肺组织胶原纤维沉积、炎性细胞浸润明显。与哮喘组比较,各药物组大鼠的咳嗽次数均明显减少(P均<0.05),地塞米松组和祛风扶阳汤高剂量组肺泡灌洗液中IL-6、IL-17A、TGF-β_(1)水平和肺组织中TGF-β_(1)、α-SMA、p-Smad2/3蛋白相对表达量及IL-17A^(+)CD4^(+)比例均明显降低(P均<0.05),地塞米松组和祛风扶阳汤高剂量组肺泡灌洗液中IL-10水平和祛风扶阳汤高剂量组肺组织中CD4^(+)CD25^(+)Foxp3^(+)Treg比例均明显升高(P均<0.05);各药物组肺组织损伤、胶原纤维沉积、炎性细胞浸润均减轻。结论祛风扶阳汤可以通过调节TGF-β_(1)/Smad信号通路以及Th17/Treg细胞平衡,从而减轻支气管哮喘大鼠气道炎症反应与气道重塑。 展开更多
关键词 哮喘 祛风扶阳汤 转化生长因子-β_(1)/smad信号通路 辅助性T细胞17 调节性T细胞
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针刺联合穴位贴敷治疗中晚期食管癌疗效观察及对楔状组织中TGF-β_(1)/Smad信号通路的影响
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作者 张慧 张娟 《新中医》 CAS 2024年第12期163-170,共8页
目的:观察针刺联合穴位贴敷治疗中晚期食管癌的临床疗效及对楔状组织中转化生长因子β_(1)(TGF-β_(1))/胰腺癌缺失因子(Smad)信号通路的影响。方法:将90例中晚期食管癌患者随机分为对照组与治疗组各45例。对照组给予常规放化疗治疗,治... 目的:观察针刺联合穴位贴敷治疗中晚期食管癌的临床疗效及对楔状组织中转化生长因子β_(1)(TGF-β_(1))/胰腺癌缺失因子(Smad)信号通路的影响。方法:将90例中晚期食管癌患者随机分为对照组与治疗组各45例。对照组给予常规放化疗治疗,治疗组在对照组基础上给予针刺联合穴位贴敷。观察2组治疗后临床疗效,不良反应及随访3年生存率;以及治疗前后简体中文版生活质量评估表(QLQ-C30)、SF-36健康调查量表[躯体功能(PCS)、社会功能(PSS)和情绪角色(MCS)]评分,血清肿瘤标志物[糖类抗原19-9(CA19-9)、癌胚抗原(CEA)、细胞角蛋白19片段抗原21-1(CYFRA21-1)、糖类抗原125(CA125)]、血清胃肠激素[血管活性肠(VIP)、生长抑素(SOM)、胃动素(MTL)、5-羟色胺(5-HT)]、楔状组织上清液中TGF-β_(1)/Smad信号通路(TGF-β_(1)RⅠ型受体、TGF-β_(1)RⅡ型受体、Smad4、Smad7)水平。结果:治疗后,治疗组疾病控制率为95.24%,对照组为73.17%,2组比较,差异有统计学意义(P<0.05)。治疗1、2个疗程,2组PCS、PSS、MCS评分均较治疗前升高(P<0.05),且治疗组相同时间点PCS、PSS、MCS评分均高于对照组(P<0.05)。治疗1、2个疗程,治疗组相同时间点QLQ-C30评分均低于对照组(P<0.05),但对照组QLQ-C30评分治疗前后比较,差异无统计学意义(P>0.05)。治疗1、2个疗程,2组CA19-9、CEA(对照组第1疗程CEA指标除外)、CYFRA21-1、CA125水平均较治疗前降低(P<0.05),且治疗组相同时间点4项指标均低于对照组(P<0.05)。治疗1、2个疗程,2组VIP、SOM、5-HT水平均较治疗前降低(P<0.05),MTL水平均较治疗前升高(P<0.05);且治疗组相同时间点VIP、SOM、5-HT水平均低于对照组(P<0.05),MTL水平均高于对照组(P<0.05)。治疗1、2个疗程,治疗组TGF-β_(1)RⅠ型受体、TGF-β_(1)RⅡ型受体、Smad4和Smad7水平均较治疗前降低(P<0.05),且相同时间点均低于对照组(P<0.05);对照组TGF-β_(1)RⅠ型受体、TGF-β_(1)RⅡ型受体、Smad7水平治疗前后差异均无统计学意义(P>0.05);对照组仅有Smad4水平于治疗2个疗程后明显低于治疗前(P<0.05)。随访3年,治疗组生存率为78.57%,对照组为56.10%,2组比较,差异有统计学意义(P<0.05)。治疗期间,治疗组骨髓抑制、皮肤毒性反应、消化道反应发生率低于对照组(P<0.05);2组膀胱、肾、心功能损伤发生率比较,差异无统计学意义(P>0.05)。结论:针刺联合穴位贴敷可明显提高中晚期食管癌放化疗患者的生存时间和生活质量,改善血清肿瘤标志物和胃肠激素水平,且安全性较高,其作用机制可能与调节TGF-β_(1)/Smad信号通路有关。 展开更多
关键词 食管癌 放化疗 针刺 穴位贴敷 血清肿瘤标志物 tgf-β_(1)/smad信号通路
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Experimental study of TGF-β1/Smads pathway inhibition of macrophage polarization based on miR145-5P negative feedback regulation
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作者 WANG Qing‑qing SHEN Xi +8 位作者 WAN Lei FAN Hai‑xia LIU Tian‑yang LI Ming LIU Lei GE Yao FAN Wen‑jie FEI Chen‑chen ZHOU Qian 《Journal of Hainan Medical University》 2022年第23期43-49,共7页
imbalance of synovial macrophages in patients with rheumatoid arthritis(RA).Methods:Human mononuclear cells(THP‑1)at logarithmic growth stage were induced into M1‑type macrophages,and RA synovial fibroblasts M1‑type m... imbalance of synovial macrophages in patients with rheumatoid arthritis(RA).Methods:Human mononuclear cells(THP‑1)at logarithmic growth stage were induced into M1‑type macrophages,and RA synovial fibroblasts M1‑type macrophages were co‑cultured into synovial macrophages.Synovial macrophages were divided into four groups:RA group(blank group),TGF‑β1 group(model group)and miR145‑5P overexpression group(TGF‑β1+miR145‑5P mimics group)and miR145‑5P overexpression negative control group(TGF‑β1+miR145‑5P‑mimics‑NC group).The blank group did not receive any treatment,and the other three groups were induced by TGF‑β1 in the medium for 48 h.Transfection miR145‑5p mimic and miR145‑5P‑mimics‑NC were added to co‑culture medium,and IL‑6,IL‑6 and IL‑6 of synovial macrophages were detected by ELISA.CD163 expression.Rt‑qpcr was used to detect miR145‑5p mRNA,TGF‑β1mRNA,Smad3mRNA,Smad7mRNA expression level.The expression of TGF‑β1/Smads pathway related proteins was detected by Western Blotting.Results:Compared with blank group,IL‑6 level was up‑regulated(P<0.01),and CD163 level was down‑regulated in model group(P<0.05),suggesting that TGF‑β1 could induce intensified immune inflammatory response.Compared with the negative miR145‑5P overexpression control group and model group,The expression of miR145‑5P overexpression group molecule CD163 was significantly increased by ELISA(P<0.01),and the expression of inflammatory factor IL‑6 was decreased(P<0.05).PCR showed that miR145‑5P mRNA expression level was significantly increased in miR145‑5P overexpression group,Smad3 mRNA and TGF‑β1 mRNA were significantly decreased,and Smad7 mRNA was significantly increased(P<0.01).WB method showed that the anti‑inflammatory protein Smad7 was significantly increased,while TGF‑β1 and Smad3 were significantly decreased(P<0.01).Transwell chamber results confirmed that miR145‑5P overexpression group significantly reduced macrophage invasion(P<0.01).Correlation analysis showed that miR145‑5P was negatively correlated with Smad3 and positively correlated with Smad7(P<0.01).Conclusion:miR145‑5P may inhibit macrophage polarization in RA patients by targeting Smad3 protein,negatively regulating TGF‑β1/Smads pathway,and alleviating immune inflammation. 展开更多
关键词 Rheumatoid arthritis miR145‑5p tgf‑β1/smads pathways Macrophage polarization In vitro studies
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积雪草苷对HSFB miR-564及其介导的TGF-β_(1)/Smad信号通路的影响 被引量:5
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作者 王瑶 袁锐 +1 位作者 刘国良 袁星星 《中医药学报》 CAS 2021年第8期32-36,共5页
目的:探讨积雪草苷对人增生性瘢痕成纤维细胞(HSFB)中miR-564及其介导的TGF-β_(1)/Smad信号通路中相关蛋白表达的影响。方法:HSFB分为对照组、0.05mg/mL、0.1mg/mL、0.5mg/mL和1mg/mL组,其中对照组加入100μL的DMEM培养基进行培养,0.05... 目的:探讨积雪草苷对人增生性瘢痕成纤维细胞(HSFB)中miR-564及其介导的TGF-β_(1)/Smad信号通路中相关蛋白表达的影响。方法:HSFB分为对照组、0.05mg/mL、0.1mg/mL、0.5mg/mL和1mg/mL组,其中对照组加入100μL的DMEM培养基进行培养,0.05mg/mL、0.1mg/mL、0.5mg/mL和1mg/mL积雪草苷组分别加入含相应浓度AS的DMEM培养基继续培养。分别采用MTT法检测细胞增殖能力,流式细胞术检测细胞凋亡水平,酶联免疫吸附试验检测细胞MMP-2、COLⅠ和COLⅢ的表达水平,免疫荧光检测细胞α-SMA蛋白的表达,RT-PCR法检测细胞中miR-564的表达,Westernblot检测TGF-β_(1)/Smad信号通路中相关蛋白的表达。结果:与对照组相比,积雪草苷干预后HSFB增殖水平显著降低,凋亡水平显著增加,细胞中MMP-2、COL-Ⅰ、COL-Ⅲ、α-SMA、TGF-β_(1)、p-Smad2,p-Smad3蛋白的表达和miR-564的表达均明显降低,差异均具有统计学意义(P<0.05或P<0.01),其中以1mg/mL组对HSFB作用最佳。结论:积雪草苷能够通过抑制HSFB中miR-564的表达,进而抑制TGF-β_(1)/Smad信号通路的激活,达到促进细胞凋亡、抑制细胞增殖和胶原分泌的作用。 展开更多
关键词 积雪草苷 人增生性瘢痕成纤维细胞 miR-564 tgf-β_(1)/smad信号通路
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红树莓提取物通过TGF-β1/Smad信号通路改善大鼠酒精性肝纤维化 被引量:3
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作者 李彤 李红灵 +3 位作者 胡浩 谢晓君 叶莉娜 兰梅 《贵州医药》 CAS 2021年第11期1686-1688,F0003,共4页
目的研究红树莓提取物对乙醇诱导的酒精性肝纤维化大鼠的保护作用及其机制。方法取SD雄性大鼠60只,随机分为6组,每组10只,分别为空白组、模型组、红树莓低浓度组(0.05 g/kg)、红树莓中浓度组(0.125 g/kg)、红树莓高浓度组(0.259 g/kg)... 目的研究红树莓提取物对乙醇诱导的酒精性肝纤维化大鼠的保护作用及其机制。方法取SD雄性大鼠60只,随机分为6组,每组10只,分别为空白组、模型组、红树莓低浓度组(0.05 g/kg)、红树莓中浓度组(0.125 g/kg)、红树莓高浓度组(0.259 g/kg)、安珐特阳性药物组(21.6 mg/kg)。通过给大鼠连续灌胃5%乙醇8 g/kg 12周构建大鼠酒精性肝纤维化模型。药物组在模型构建成功后分别按剂量灌胃给药,1次/d,持续给药4周,末次给药后采集血液和肝脏组织。HE和Masson染色观察各组肝脏病理变化,检测血清中ALT,AST和TC的含量,检测肝脏中TGF-β1和Smad7的蛋白表达。结果HE染色和Masson染色结果表明模型组大鼠肝组织结构破坏,肝细胞出现变性坏死,可见脂肪变性,汇管区及中央静脉区炎性细胞浸润,大量的胶原沉积。与模型组比较,红树莓低、中、高浓度组和安珐特组中肝组织破坏程度降低,肝细胞变性程度减轻,汇管区炎性细胞浸润减少,胶原沉积也显著减少,且红树莓浓度越高,改善程度越显著。与模型组比较,红树莓低、中、高浓度组和安珐特组大鼠血清中ALT、AST和TC水平显著降低(P<0.05),肝脏组织中TGF-β1蛋白表达显著降低,Smad7表达显著升高(P<0.05)。结论树莓提取物可通过TGF-β1/Smad信号通路实现对酒精性肝损害的保护作用。 展开更多
关键词 红树莓提取物 酒精性肝纤维化 大鼠 tgf1 smad 信号通路
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中药软肝饮对CCl_4诱导的肝纤维化大鼠TGF-1/Smad信号通路的影响 被引量:5
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作者 林红 张国梁 《浙江中医药大学学报》 CAS 2008年第2期169-171,共3页
[目的]研究中药软肝饮对CCl4诱导的大鼠肝纤维化肝脏TGF-1及Smad3,Smad7表达的影响,探讨其抗纤维化的作用机制。[方法]Wistar大鼠40只,随机分成正常对照组,模型对照组,软肝饮治疗组,鳖甲软肝片对照组,采用CCl4背部皮下注射构建肝纤维化... [目的]研究中药软肝饮对CCl4诱导的大鼠肝纤维化肝脏TGF-1及Smad3,Smad7表达的影响,探讨其抗纤维化的作用机制。[方法]Wistar大鼠40只,随机分成正常对照组,模型对照组,软肝饮治疗组,鳖甲软肝片对照组,采用CCl4背部皮下注射构建肝纤维化模型,行HE和VG染色,光镜下观察肝组织肝纤维化程度。同时免疫组化SABC方法检测各组TGF-1、Smad3和Smad7的表达。[结果]与正常对照组相比,模型组TGF-1、Smad3表达明显增强,Smad7表达明显下降。经软肝饮治疗后大鼠肝脏TGF-1表达比模型组减弱。软肝饮同时下调Smad3的表达,上调Smad7的表达。另外,软肝饮组大鼠肝脏病理变化显著改善。[结论]肝炎平对大鼠肝纤维化肝脏TGF-1/Smad信号通路有明显的影响,能抑制CCl4诱导的大鼠肝纤维化,其作用机制可能为抑制TGF-1表达,下调Smad3及上调Smad7的表达。 展开更多
关键词 软肝饮 tgf-1/smad信号通路 肝纤维化
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TGF-β/Smad信号转导通路对紫外线致人工皮肤光损伤中MMP-1、pro-collagen Ⅰ mRNA表达影响的初步研究 被引量:5
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作者 罗雯 姚露 +2 位作者 顾华 涂颖 何黎 《皮肤病与性病》 2011年第3期125-128,共4页
目的探讨人工皮肤光损伤中TGF-β/Smad信号转导通路与基质金属蛋白酶1及Ⅰ型前胶原蛋白的相互作用。方法以紫外线照射人工皮肤后,通过Real-Time RT-PCR法(荧光染料掺入法)检测其中基质金属蛋白酶1、Ⅰ型前胶原蛋白、TGFβRⅠ及TGFβRⅡm... 目的探讨人工皮肤光损伤中TGF-β/Smad信号转导通路与基质金属蛋白酶1及Ⅰ型前胶原蛋白的相互作用。方法以紫外线照射人工皮肤后,通过Real-Time RT-PCR法(荧光染料掺入法)检测其中基质金属蛋白酶1、Ⅰ型前胶原蛋白、TGFβRⅠ及TGFβRⅡmRNA的表达量。结果紫外线使人工皮肤中基质金属蛋白酶1(MMP-1)的mRNA表达量明显增加,而Ⅰ型前胶原蛋白mRNA的表达下调(P<0.05),TGFβRⅡmRNA表达显著下调(P<0.01);加入TGF-β1后MMP-1表达显著下调(P<0.01),Ⅰ型前胶原蛋白及TGFβRⅡmRNA表达显著增高(P<0.01);而UV照射后8小时加入TGF-β1,MMP-1表达量较对照组高(P<0.05),Ⅰ型前胶原蛋白及TGFβRⅡmRNA表达量均较对照组低(P<0.05)。结论 UV可以抑制人工皮肤中Ⅰ型前胶原mRNA的表达、上调MMP-1的表达,而这种调控作用可能与TGF-βRⅡ的表达受抑制,TGF-β/Smad信号传导通路被削弱有关。 展开更多
关键词 紫外线 人工皮肤 Ⅰ型前胶原 基质金属蛋白酶-1 tgf-β/smad信号传导通路
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丹玄口康对ANE诱导的口腔黏膜下纤维化TGFβ1/Smad信号通路的影响 被引量:8
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作者 谭劲 岳金宝 +3 位作者 罗玉姣 吴丹 刘寻 李群 《中国医药科学》 2018年第5期27-31,71,共6页
目的探讨丹玄口康对ANE诱导的口腔黏膜下纤维化TGFβ_1/Smad信号通路的影响。方法体外培养大鼠口腔黏膜FB,以ANE为诱导剂,丹玄口康药物血清为干预物,以TGFβ_1/Smad信号通路阻断剂LY2109761为阳性对照物,采用免疫细胞化学法检测细胞内... 目的探讨丹玄口康对ANE诱导的口腔黏膜下纤维化TGFβ_1/Smad信号通路的影响。方法体外培养大鼠口腔黏膜FB,以ANE为诱导剂,丹玄口康药物血清为干预物,以TGFβ_1/Smad信号通路阻断剂LY2109761为阳性对照物,采用免疫细胞化学法检测细胞内Ⅰ型胶原蛋白、磷酸化Smad2/3蛋白的表达变化,用酶联免疫吸附剂测定法检测培养上清Ⅰ型胶原的含量,采用荧光定量PCR检测Ⅰ型胶原m RNA的表达变化。结果 ANE刺激FB后,细胞和上清液中Ⅰ型胶原的表达、Smad2/3的磷酸化胞核的转位水平和Ⅰ型胶原m RNA的表达均高于正常组(P<0.05);ANE刺激FB的同时给予LY2109761干预后,细胞和上清液中Ⅰ型胶原的表达、磷酸化Smad2/3的胞核转位水平和Ⅰ型胶原m RNA的表达均有所降低(P<0.05);ANE刺激FB的同时给予丹玄口康含药血清干预后,细胞和上清液中I型胶原的表达、磷酸化Smad2/3的胞核转位水平和I型胶原m RNA的表达均有所降低(P<0.05)。结论丹玄口康可通过调控TGFβ_1/Smads信号转导通路,抑制ANE刺激的FB胶原蛋白的合成,从而发挥抗纤维化作用。 展开更多
关键词 丹玄口康 口腔黏膜下纤维化 Ⅰ型胶原蛋白 tgfβ1/smad信号通路
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基于TGF-β_(1)/Smads信号通路中医药治疗骨质疏松症的实验研究进展 被引量:7
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作者 张国光 杨杰 +3 位作者 于冬冬 顾明 马韬 杨鸫祥 《中华中医药学刊》 CAS 北大核心 2021年第9期151-155,共5页
目的综述近年来中医药基于TGF-β_(1)/Smads信号通路治疗骨质疏松症的实验研究进展。方法检索近年来国内外公开发表的相关文献,从该信号通路激活后调控骨代谢、治疗骨质疏松症层面,分别总结中药提取物、中药复方制剂和中医外治法治疗骨... 目的综述近年来中医药基于TGF-β_(1)/Smads信号通路治疗骨质疏松症的实验研究进展。方法检索近年来国内外公开发表的相关文献,从该信号通路激活后调控骨代谢、治疗骨质疏松症层面,分别总结中药提取物、中药复方制剂和中医外治法治疗骨质疏松症的作用机制。结果相关实验研究主要集中于TGFβ_(1)-Smads、TGFβ_(1)-BMPs这两条信号通路,且中医药通过该通路对骨质疏松模型的治疗均取得较好实验结果。结论通过对TGF-β_(1)/Smads信号通路的实验研究,在分子水平阐释了中医药治疗骨质疏松症的作用机制。 展开更多
关键词 中医药 tgf-β_(1)/smads 骨质疏松症 信号通路 实验研究
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抑制TGF-β_(1)/Smads通路中Smad7泛素化降解改善小鼠肺纤维化的作用机制 被引量:6
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作者 杨珣 邵松军 +3 位作者 崔妙雅 李霜 张湘燕 饶珊珊 《山东医药》 CAS 2022年第17期47-51,共5页
目的探讨抑制TGF-β_(1)/Smads通路中Smad7泛素化降解改善小鼠肺纤维化的作用机制。方法将30只雄性C57小鼠按随机数表法分为对照组、模型组及MG132干预组,每组10只。模型组及MG132干预组采用一次性气管滴入博来霉素构建肺纤维化模型,空... 目的探讨抑制TGF-β_(1)/Smads通路中Smad7泛素化降解改善小鼠肺纤维化的作用机制。方法将30只雄性C57小鼠按随机数表法分为对照组、模型组及MG132干预组,每组10只。模型组及MG132干预组采用一次性气管滴入博来霉素构建肺纤维化模型,空白组小鼠不做处理。MG132干预组于造模第2天起给予Smad7泛素蛋白酶体抑制剂MG132腹腔注射,对照组及模型组给予等量生理盐水腹腔注射。28 d后观察各组小鼠肺纤维化程度(HE染色观察肺组织形态学、Masson染色观察肺组织胶原含量、ELISA检测肺组织羟脯氨酸含量);Western blotting法检测小鼠肺组织α-SMA、Smad7、CollagenⅠ蛋白表达;qRT-PCR法检测小鼠肺组织α-SMA、Smad7、CollagenⅠ、TGF-β_(1) mRNA表达;免疫沉淀Smad7蛋白,免疫印迹检测各组小鼠肺组织中Smad7泛素化水平。结果HE染色结果显示,对照组小鼠肺组织结构完整,模型组小鼠肺组织正常结构遭到破坏,MG132干预组小鼠肺组织结构破坏程度减轻;Masson染色结果显示,对照组镜下蓝紫色面积(胶原纤维沉积)最小,模型组镜下见大片蓝紫色视野,MG132干预组蓝紫色视野面积较模型组缩小;羟脯氨酸含量检测结果显示,小鼠肺组织羟脯氨酸含量模型组>MG132干预组>对照组(P均<0.05)。各组小鼠肺组织α-SMA、CollagenⅠ蛋白表达比较,模型组>MG132干预组>对照组;Smad7蛋白表达比较,对照组>MG132干预组>模型组(P均<0.05)。各组小鼠肺组织α-SMA、Smad7、CollagenⅠ、TGF-β_(1) mRNA表达比较,模型组>MG132干预组>对照组(P均<0.05)。各组小鼠肺组织Smad7泛素化水平比较,模型组>MG132干预组>对照组。结论抑制Smad7泛素化降解可通过上调Smad7蛋白水平增强Smad7对TGF-β1/Smads信号通路的负向调控作用,减轻肺纤维化病变。 展开更多
关键词 肺纤维化 MG132 泛素化 smad7 tgf-β_(1)/smads信号通路
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血管损伤后TGF-β1/Smad信号通路在诱导BMSCs分化参与血管再狭窄的相关性研究 被引量:3
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作者 郑仕杰 周敬群 +4 位作者 杨维华 黄迪 蔡金丹 戴秋婷 吕建峰 《中国医药科学》 2019年第17期50-54,共5页
目的观察转化生长因子-β1(TGF-β1)与骨髓间充质干细胞(BMSCs)在血管损伤后新生内膜中的表达,研究TGF-β1与BMSCs参与新生内膜修复的关系。方法选择右侧颈动脉内膜损伤的大鼠模型,实验分为6组,分别为对照组和实验组(实验组分5组:损伤0h... 目的观察转化生长因子-β1(TGF-β1)与骨髓间充质干细胞(BMSCs)在血管损伤后新生内膜中的表达,研究TGF-β1与BMSCs参与新生内膜修复的关系。方法选择右侧颈动脉内膜损伤的大鼠模型,实验分为6组,分别为对照组和实验组(实验组分5组:损伤0h、3d、7d、14d、21d组)。选取实验组各时间点的损伤血管组织,采用HE染色了解内膜增生导致损伤血管的狭窄水平,同时通过Westernblot法检测TGF-β1、p-Smad2/3、Smad2/3蛋白的表达、BMSCs标记物蛋白(Nestin)的表达,并检测与增殖标记物Ki-67的表达关系。结果(1)血管损伤后的不同时间点检测到新生内膜有不同程度的增生,以损伤组7d、14d、21d组新生内膜增生显著,与时间呈正相关,三组间比较差异有统计学意义(P<0.05);对照组与实验组(0h、3d组)未见新生内膜增生。(2)实验7d组的新生内膜中TGF-β1、p-Smad2/3、Smad2/3蛋白表达量开始升高,实验14d组达最高值,实验21d组表达量下降;且蛋白表达量与细胞增殖标记物Ki-67阳性指数呈正相关。(3)Western Blot法检测BMSCs标记物Nestin蛋白仅在7d、14d组中表达,并与TGF-β1的表达量正相关。结论(1)TGF-β1对血管损伤后内膜增生的促进作用可能通过Smad经典信号通路;(2)损伤血管的重建可能与TGF-β1的分泌招募BMSCs集聚损伤处有关,并诱导BMSCs向内膜细胞分化,最终共同参与新生内膜的形成。 展开更多
关键词 tgf1/smad信号通路 骨髓间充质干细胞 血管损伤
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散结消瘤方调控TGF-β_(1)/Smads介导的上皮间质转化对乳腺癌皮下移植瘤的影响 被引量:2
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作者 陈茂 欧阳灿 《现代中西医结合杂志》 CAS 2023年第5期615-620,695,共7页
目的探讨散结消瘤方通过调节转化生长因子-β_(1)(TGF-β_(1))/Smads信号通路及其介导的上皮间质转化(EMT)对小鼠乳腺癌皮下移植瘤的影响。方法雌性BALB/cA裸小鼠40只,按体重随机分为模型组、环磷酰胺组、散结消瘤方低剂量组、散结消瘤... 目的探讨散结消瘤方通过调节转化生长因子-β_(1)(TGF-β_(1))/Smads信号通路及其介导的上皮间质转化(EMT)对小鼠乳腺癌皮下移植瘤的影响。方法雌性BALB/cA裸小鼠40只,按体重随机分为模型组、环磷酰胺组、散结消瘤方低剂量组、散结消瘤方中剂量组、散结消瘤方高剂量组,每组8只。各组均采用人乳腺癌细胞株(MCF-7)接种法制备乳腺癌皮下移植瘤模型。造模第6天,环磷酰胺组给予环磷酰胺溶液30 mg/kg腹腔注射,散结消瘤方低、中、高剂量组分别给予7.8 g/kg、15.6 g/kg、31.2 g/kg散结消瘤方灌胃,模型组给予生理盐水灌胃,均持续干预4周。比较各组小鼠瘤重和抑瘤率,免疫组化染色观察瘤组织中基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)阳性表达情况,Western blot法检测肿瘤组织中E-cadherin、Vimentin、twist、Snail、TGF-β_(1)、Smad2、p-Smad2、Smad3、p-Smad3蛋白表达情况,RT-PCR法检测肿瘤组织中TGF-β_(1)、Smad2、Smad3 mRNA表达情况。结果环磷酰胺组及散结消瘤方各组瘤重均明显低于模型组(P均<0.05);散结消瘤方高剂量组和环磷酰胺组瘤重均明显低于散结消瘤方低、中剂量组(P均<0.05),抑瘤率均明显高于散结消瘤方低、中剂量组(P均<0.05)。环磷酰胺组及散结消瘤方各组瘤组织中MMP-2、MMP-9阳性表达平均光密度值,Vimentin、twist、Snail、TGF-β_(1)蛋白相对表达量及p-Smad2/Smad2、p-Smad3/Smad3比值,TGF-β_(1)、Smad2、Smad3 mRNA相对表达量均明显低于模型组(P均<0.05),瘤组织中E-cadherin蛋白相对表达量均明显高于模型组(P均<0.05);散结消瘤方高剂量组和环磷酰胺组上述各指标改善情况均明显优于散结消瘤方低、中剂量组(P均<0.05),散结消瘤方高剂量组与环磷酰胺组各指标比较差异均无统计学意义(P均>0.05)。结论散结消瘤方对乳腺癌皮下移植瘤具有明显的抑瘤作用,其作用机制可能与调控TGF-β_(1)/Smads信号通路,逆转其所介导的EMT相关。 展开更多
关键词 乳腺癌 散结消瘤方 上皮间质转化 转化生长因子-β_(1)/smads信号通路
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调控TGFβ1/SMAD通路的microRNAs在失神经支配骨骼肌中的表达
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作者 刘非 张丹丹 +3 位作者 陈东辉 宋先敏 刘菲 郑宏良 《解剖学杂志》 CAS CSCD 北大核心 2016年第3期319-323,共5页
目的:本研究拟探讨骨骼肌失神经支配后差异性表达的microRNAs,并明确其是否参与调控TGFβ1/SMAD信号通路.方法:C57/BL6J小鼠,随机分为正常对照组和实验组,实验组小鼠切断右下肢坐骨神经为手术组,左下肢游离坐骨神经作为假手术组.4周... 目的:本研究拟探讨骨骼肌失神经支配后差异性表达的microRNAs,并明确其是否参与调控TGFβ1/SMAD信号通路.方法:C57/BL6J小鼠,随机分为正常对照组和实验组,实验组小鼠切断右下肢坐骨神经为手术组,左下肢游离坐骨神经作为假手术组.4周后处死小鼠取腓肠肌Masson染色观察肌纤维形态变化,比较各组肌纤维横截面积.以TGFβ1/SMAD为靶基因,通过生物信息学分析寻找到18个可能的miRNAs指标.定量PCR检测其表达,并针对表达升高的microRNAs采用荧光素酶报告基因实验确认其靶基因.结果:手术组肌纤维横截面积比对照组明显缩小,对照组与假手术组肌肉之间的差异无统计学意义.在失神经骨骼肌中特异性高表达的有miR-424、miR-744、miR-15a.在C2C12细胞系中行报告基因实验显示,与对照组比较,转染miR-744后,SMAD3的荧光素酶强度下降;转染miR-15a后,TGFβ1的荧光素酶强度下降;转染miR-424后,SMAD3的荧光素酶强度变化无统计学意义.PCR验证microRNAs的靶基因显示,转染miR-744、miR-15a的模拟物后,分别对应的SMAD3、TGFβ1表达下调,差异有统计学意义.结论:miR-424、miR-744、miR-15a可能参与调控失神经支配导致的骨骼肌萎缩纤维化,其中miR-744的靶基因是SMAD3,miR-15a的靶基因是TGFβ1. 展开更多
关键词 骨骼肌 mRNA TGβ1/smad信号通路 失神经 肌纤维化
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