Objective To investigate the role of transforming growth factor-β1 （TGF-β1）, Smad2/3 and Smad7 expressions in carotid artery remodeling in renovascular hypertensive rats, and also the therapeutic effect of Enalapr...Objective To investigate the role of transforming growth factor-β1 （TGF-β1）, Smad2/3 and Smad7 expressions in carotid artery remodeling in renovascular hypertensive rats, and also the therapeutic effect of Enalapril and Amlodipine. Methods The renovascular hypertensive rat （RHR） models with ＂two-kidney and one-clip＂ were established, including model group （n = 6）, sham-operated group （n = 6）, Enalapril group （10 mg/kg per day, n = 6）, Amlodipine group （5 mg/kg per day, n = 6） and combination group （Amlodipine 2.5 mg/kg per day ＋ Enalapril 5mg/kg per day, n = 6）. The medication were continuous administrated for six weeks. Carotid artery morphological and structural changes in the media were observed by HE staining, Masson staining and immuno histochemical staining. Media thickness （MT）, MT and lumen diameter ratio （MT/LD）, and the expression levels of media a-smooth muscle actin （α-actin）, proliferating cell nuclear antigen （PCNA）, TGF-β1, phosphorylated Smad2/3 （p-Smad2/3） and Smad7 in carotid arteries were measured. Results The media of carotid arteries in RHR model group was significantly thickened, the volume of smooth muscle cell was increased, and the array was in disorder; MT, MT/LD, the proliferation index of smooth muscle cell and collagen fiber area percentage of carotid arteries in the model group were significantly higher than those in the sham-operated group （P 〈 0.01）. Compared to sham-operated group, the model group had significantly higher expressions of TGF-β1 and p-Smad2/3 （P 〈 0.05） and lower Smad7 expression. Both Enalapril and Amlodipine improved smooth muscle hypertrophy and collagen deposition, reduced RHR carotid MT, MT/LD, proliferation index of smooth muscle cell, collagen fiber area percentage and the expressions of TGF-β1 and p-Smad2/3 （P 〈 0.05）, increased Smad7 expression （P 〈 0.05）. Moreover, the combination treatment of Enalapril and Amlodipine had significantly better effects than single Amlodipine group （P 〈 0.05）, but not single Enalapril group. Conclusions TGF-β1/Smads pathway may participate in the mechanism of carotid artery remodeling in RHR; the role of Amlodipine and Enalapril in inversing carotid artery remodeling may be related to the change of TGF-β1/Smads pathway, the combination treatment of Amlodipine and Enalapril had better effects than single administration of Amlodipine.展开更多
Objective: To investigate the inhibitory effect of apogossypolone (ApoG2) on prostate cancer cell line PC-3 in vivo, and explore its mechanism. Methods: The models of transplantation tumors in Balb/c nu/nu mice were e...Objective: To investigate the inhibitory effect of apogossypolone (ApoG2) on prostate cancer cell line PC-3 in vivo, and explore its mechanism. Methods: The models of transplantation tumors in Balb/c nu/nu mice were established via subcutaneous injection of PC-3 cells and the tumor-transplanted mice were divided into 4 groups: control group and three ApoG2 treatment groups, with 10 mice in each group. Volumes of the tumor were estimated every 2 d and the morphology of tumor tissues was observed. Immunohistochemistry was employed to observe the expression of Bcl-2, PCNA, CD31, caspase-3 and caspase-8 in tumor tissues. Results: ApoG2 (2.5 mg/kg-10 mg/kg) given intraperitoneally once a day can obviously inhibit the growth of subcutaneous prostatic carcinoma implant. The tumor volume decreased obviously when the treatment dosage was bigger than 5.0 mg/kg (P<0.01). Meanwhile, ApoG2 decreased the expression of PCNA and CD31, and enhanced the expression of caspases-3, caspase-8 in tumor tissues. Conclusion: ApoG2 exert an inhibitory effect on prostatic carcinoma possibly by inducing apoptosis and inhibiting tumor angiogenesis.展开更多
Objective: To investigate the correlation between the gastric mucosal cell proliferation and low-concentration alcohol intake in a chronic drinking rat model, and to investigate the possible role of ROS/BMK1 pathway i...Objective: To investigate the correlation between the gastric mucosal cell proliferation and low-concentration alcohol intake in a chronic drinking rat model, and to investigate the possible role of ROS/BMK1 pathway in this process. Methods: SD rats were randomly divided into 4 groups: control group, administered with tap water; ethanol group, with 6% ethanol in the drinking water; quercetin group, with quercetin (100 mg/kg) by intragastric gavage twice a day; ethanol+quercetin group, administered with quercetin combined with 6% ethanol. The cell proliferation in rat gastric mucosa was analyzed by flow cytometery and proliferating cell nuclear antigen (PCNA) immunohistochemical staining. Activation of ERKs and BMK1 was evaluated by the expression and phosphorylation of these kinases using Western Blot analysis. Results: Compared to the controls, the cell proliferation in gastric mucosa of rats exposed to the ethanol for 7 d was enhanced, and the activation of BMK1 was also increased in this period. Otherwise quercetin, as a free radical scavenger, attenuated increased cell proliferation and activation of BMK1 in rat stomach treated with ethanol. However, no changes of ERKs expression and phosphorylation occurred in the rats in all groups. Conclusion: These results suggested that the ROS and BMK1 activation may be a central mechanism, which underlies cell proliferation in rat gastric mucosa stimulus with the chronic low-concentration ethanol.展开更多
Objective：To evaluate the effects of curcumin on regulating the proliferation,cell cycle distribution,apoptosis and relevant mechanisms in keratinocyte cell lines.Methods：The human immortalized human keratinocyte li...Objective：To evaluate the effects of curcumin on regulating the proliferation,cell cycle distribution,apoptosis and relevant mechanisms in keratinocyte cell lines.Methods：The human immortalized human keratinocyte lines（HaCaT cells） were treated with different doses of curcumin.The effects of curcumin on cell viability were measured by MTT assay,and the cell cycle distribution and apoptosis determined by flow cytometry.The mRNA expression changes of proliferating cell nuclear antigen（PCNA）,cyclin D1 and Bcl-xL were from real-time PCR analysis and the protein levels were detected by Western blotting.Results：Data obtained in the study showed that curcumin could cause significantly inhibitory effect on proliferation in HaCaT cells in a time- and dose-dependent manner.Cell arrest at G1/S phase and significant apoptosis were observed after being treated with curcumin for 24 h.In association with these,the expression of PCNA,cyclin D1 and Bcl-xL were decreased both at mRNA and protein levels for the same treatment.Conclusion：Curcumin can inhibit proliferation,induce cell arrest at G1/S phase and cause apoptosis in HaCaT cells.The decreased expression of PCNA,cyclin D1 and Bcl-xL induced by curcumin contributes to the above effects in vitro.展开更多
Objective: To analyze the relationship of Stat3 expression with clinical stages, tissue types, p53 and proliferation cell nuclear antigen (PCNA) in human lung carcinoma, and to evaluate the role of Stat3 in the pathog...Objective: To analyze the relationship of Stat3 expression with clinical stages, tissue types, p53 and proliferation cell nuclear antigen (PCNA) in human lung carcinoma, and to evaluate the role of Stat3 in the pathogenesis of lung carcinoma. Methods: Immunohistochemical method were used to detected Stat3, p53 and PCNA in different tissues of patients (n = 42) with lung carcinoma who accepted neither radiotherapy nor chemotherapy. Results: The positive rate of StatS was 81. 0% in lung carcinoma and its expression level was related to the tissue type but not to T, N or the clinical stage. The expression level of Stat3 in non-small cell lung carcinoma (NSCLC) was higher than that in small cell lung carcinoma (SCLC). A positive correlation of the expression of Stat3 with that of p53 and PCNA was identified. Conclusion:The expression level of Stat3 is abnormal in lung carcinoma. Stat3 may be involved in the regulation of p53 gene in lung carcinoma cell, it may accelerate the proliferation of lung carcinoma cells and play an important role in the pathogenesis of lung carcinoma.展开更多
文摘Objective To investigate the role of transforming growth factor-β1 （TGF-β1）, Smad2/3 and Smad7 expressions in carotid artery remodeling in renovascular hypertensive rats, and also the therapeutic effect of Enalapril and Amlodipine. Methods The renovascular hypertensive rat （RHR） models with ＂two-kidney and one-clip＂ were established, including model group （n = 6）, sham-operated group （n = 6）, Enalapril group （10 mg/kg per day, n = 6）, Amlodipine group （5 mg/kg per day, n = 6） and combination group （Amlodipine 2.5 mg/kg per day ＋ Enalapril 5mg/kg per day, n = 6）. The medication were continuous administrated for six weeks. Carotid artery morphological and structural changes in the media were observed by HE staining, Masson staining and immuno histochemical staining. Media thickness （MT）, MT and lumen diameter ratio （MT/LD）, and the expression levels of media a-smooth muscle actin （α-actin）, proliferating cell nuclear antigen （PCNA）, TGF-β1, phosphorylated Smad2/3 （p-Smad2/3） and Smad7 in carotid arteries were measured. Results The media of carotid arteries in RHR model group was significantly thickened, the volume of smooth muscle cell was increased, and the array was in disorder; MT, MT/LD, the proliferation index of smooth muscle cell and collagen fiber area percentage of carotid arteries in the model group were significantly higher than those in the sham-operated group （P 〈 0.01）. Compared to sham-operated group, the model group had significantly higher expressions of TGF-β1 and p-Smad2/3 （P 〈 0.05） and lower Smad7 expression. Both Enalapril and Amlodipine improved smooth muscle hypertrophy and collagen deposition, reduced RHR carotid MT, MT/LD, proliferation index of smooth muscle cell, collagen fiber area percentage and the expressions of TGF-β1 and p-Smad2/3 （P 〈 0.05）, increased Smad7 expression （P 〈 0.05）. Moreover, the combination treatment of Enalapril and Amlodipine had significantly better effects than single Amlodipine group （P 〈 0.05）, but not single Enalapril group. Conclusions TGF-β1/Smads pathway may participate in the mechanism of carotid artery remodeling in RHR; the role of Amlodipine and Enalapril in inversing carotid artery remodeling may be related to the change of TGF-β1/Smads pathway, the combination treatment of Amlodipine and Enalapril had better effects than single administration of Amlodipine.
文摘Objective: To investigate the inhibitory effect of apogossypolone (ApoG2) on prostate cancer cell line PC-3 in vivo, and explore its mechanism. Methods: The models of transplantation tumors in Balb/c nu/nu mice were established via subcutaneous injection of PC-3 cells and the tumor-transplanted mice were divided into 4 groups: control group and three ApoG2 treatment groups, with 10 mice in each group. Volumes of the tumor were estimated every 2 d and the morphology of tumor tissues was observed. Immunohistochemistry was employed to observe the expression of Bcl-2, PCNA, CD31, caspase-3 and caspase-8 in tumor tissues. Results: ApoG2 (2.5 mg/kg-10 mg/kg) given intraperitoneally once a day can obviously inhibit the growth of subcutaneous prostatic carcinoma implant. The tumor volume decreased obviously when the treatment dosage was bigger than 5.0 mg/kg (P<0.01). Meanwhile, ApoG2 decreased the expression of PCNA and CD31, and enhanced the expression of caspases-3, caspase-8 in tumor tissues. Conclusion: ApoG2 exert an inhibitory effect on prostatic carcinoma possibly by inducing apoptosis and inhibiting tumor angiogenesis.
文摘Objective: To investigate the correlation between the gastric mucosal cell proliferation and low-concentration alcohol intake in a chronic drinking rat model, and to investigate the possible role of ROS/BMK1 pathway in this process. Methods: SD rats were randomly divided into 4 groups: control group, administered with tap water; ethanol group, with 6% ethanol in the drinking water; quercetin group, with quercetin (100 mg/kg) by intragastric gavage twice a day; ethanol+quercetin group, administered with quercetin combined with 6% ethanol. The cell proliferation in rat gastric mucosa was analyzed by flow cytometery and proliferating cell nuclear antigen (PCNA) immunohistochemical staining. Activation of ERKs and BMK1 was evaluated by the expression and phosphorylation of these kinases using Western Blot analysis. Results: Compared to the controls, the cell proliferation in gastric mucosa of rats exposed to the ethanol for 7 d was enhanced, and the activation of BMK1 was also increased in this period. Otherwise quercetin, as a free radical scavenger, attenuated increased cell proliferation and activation of BMK1 in rat stomach treated with ethanol. However, no changes of ERKs expression and phosphorylation occurred in the rats in all groups. Conclusion: These results suggested that the ROS and BMK1 activation may be a central mechanism, which underlies cell proliferation in rat gastric mucosa stimulus with the chronic low-concentration ethanol.
文摘Objective：To evaluate the effects of curcumin on regulating the proliferation,cell cycle distribution,apoptosis and relevant mechanisms in keratinocyte cell lines.Methods：The human immortalized human keratinocyte lines（HaCaT cells） were treated with different doses of curcumin.The effects of curcumin on cell viability were measured by MTT assay,and the cell cycle distribution and apoptosis determined by flow cytometry.The mRNA expression changes of proliferating cell nuclear antigen（PCNA）,cyclin D1 and Bcl-xL were from real-time PCR analysis and the protein levels were detected by Western blotting.Results：Data obtained in the study showed that curcumin could cause significantly inhibitory effect on proliferation in HaCaT cells in a time- and dose-dependent manner.Cell arrest at G1/S phase and significant apoptosis were observed after being treated with curcumin for 24 h.In association with these,the expression of PCNA,cyclin D1 and Bcl-xL were decreased both at mRNA and protein levels for the same treatment.Conclusion：Curcumin can inhibit proliferation,induce cell arrest at G1/S phase and cause apoptosis in HaCaT cells.The decreased expression of PCNA,cyclin D1 and Bcl-xL induced by curcumin contributes to the above effects in vitro.
文摘Objective: To analyze the relationship of Stat3 expression with clinical stages, tissue types, p53 and proliferation cell nuclear antigen (PCNA) in human lung carcinoma, and to evaluate the role of Stat3 in the pathogenesis of lung carcinoma. Methods: Immunohistochemical method were used to detected Stat3, p53 and PCNA in different tissues of patients (n = 42) with lung carcinoma who accepted neither radiotherapy nor chemotherapy. Results: The positive rate of StatS was 81. 0% in lung carcinoma and its expression level was related to the tissue type but not to T, N or the clinical stage. The expression level of Stat3 in non-small cell lung carcinoma (NSCLC) was higher than that in small cell lung carcinoma (SCLC). A positive correlation of the expression of Stat3 with that of p53 and PCNA was identified. Conclusion:The expression level of Stat3 is abnormal in lung carcinoma. Stat3 may be involved in the regulation of p53 gene in lung carcinoma cell, it may accelerate the proliferation of lung carcinoma cells and play an important role in the pathogenesis of lung carcinoma.
