1.The stimulating effects of neuropeptide Y on cultured arterial smooth muscle cell proliferation and losartan treatment
Jiankang LIU ; Shaohua HUANG ; Minsheng CHEN
Chinese Journal of Pathophysiology 1986;0(01):-
AIM:To investigate the interplay between the neuropeptide Y(NPY) and renin-angiotensin system, and relationship to the pathogenesis of hypertension. METHODS: The method of cellular culture, MTT colorimetric assay and quantitative immunocytochemistry through ACAS570 were performed for the effect of neuropeptide Y on proliferation of cultured rat vascular smooth muscle cell (VSMC) and losartan treatment. RESULTS:It was observed that exposure of VSMC to neuropeptide Y could stimulate the proliferation of VSMC and caused increase respectively in MTT OD values and expression of proliferating cell nulear antigen(PCNA) but losartan interfered with NPY stimulating effects on VSMC and decreased MTT OD values and expression of PCNA. CONCLUSION:These results demonstrated that the NPY could promote proliferation of VSMC, this effect was partly preformed through angiotensin Ⅱ receptor.
2.The stimulating effects of neuropeptide Y on cultured arterial smooth muscle cell proliferation and losartan treatment
Shaohua HUANG ; Jiankang LIU ; Minsheng CHEN
Chinese Journal of Pathophysiology 1986;0(03):-
AIM: To observe expression of proliferating cell nuclear antigen (PCNA), platelet derived growth factor (PDGF) and c-myc in cultured vascular smooth muscle cells which is effected by neuropeptide Y (NPY) and losartan (the receptor blocking agent of angiotensin Ⅱ) therefore exploring effects of NPY on the generation of hypertension and its relationship with losartan reverse treatment in molecular biology. METHODS: Applied the method of quantitative immunocytochemistry through ACAS570. RESULTS: 24 hours exposure of vascular smooth muscle cell to NPY caused an increase in expression of PCNA, PDGF and c-myc respectively. But losartan could reverse these expressions by NPY, decreased the expression of PCNA, PDGF and c-myc. CONCLUSION: NPY is closely related to the generation of hypertension. But losartan could reverse these effects of NPY.
3.CLINICAL OBSERVATION ON THE CHANGES OF SERUM AFP BEFORE AND AFTER CRYOSURGERY FOR LIVER CANCER
Gaobin SUN ; Peng CHENG ; Minsheng LIU ;
Cancer Research and Clinic 2000;0(06):-
Objective:To study the dynamic changes of serum AFP before and after cryosurgery for liver cancer.Methods:The dynamic changes of serum AFP in 46 cases of liver cancer before and after cryosurgery were analyzed.Results:In those with a negative AFP before operation,the value of AFP increased rapidly 3 days after operation,kept positive for half a month,and was difficult to be turned negative.In those with a positive AFP before operation,there were no evident changes 3 days after operation,and the value of AFP decreased to normal half a month after operation.Conclusion:The change of AFP had some characteristic in the cryosurgery of liver cancer.Detection on the changes of AFP value is helpful in judging the curative effect and prognosis of cryosurgery for liver cancer patients.
4.C Reactive Protein Increases the Expression of Receptor for Advanced Glycation End-products in Human Endothelial Cells
Yun ZHONG ; Xiaoqing HE ; Minsheng CHEN ; Shiming LIU
Chinese Journal of Hypertension 2007;0(04):-
Objective To investigate the effect of C reactive protein on receptor of advanced glycation end-products protein (RAGE) and mRNA expression in human endothelial cells. Methods Human saphenous vein endothelial cells (HSVECs) were incubated with CRP. RAGE protein levels were determined by flow cytometry, and RAGE mRNA levels were assessed by RT-PCR. Results (1)Compared with control group (100%), CRP caused a significant increase in RAGE protein expression at a dose as low as 5 ?g/mL (175.2%?8.1%, P0.05). Conclusion C-reactive protein upregulates RAGE protein and mRNA expression in human endothelial cells in a dose and time dependent manner.
5.Ethical Considerations on the Reuse of Clinical Laboratory Blood Samples in Research
Xiaoyun CHEN ; Qian ZHANG ; Sijie WANG ; Minsheng FAN ; Sheng LIU
Chinese Medical Ethics 2016;29(4):649-651,654
By referring to the domestic and foreign relevant regulatory guidelines, this paper analyzed and sum-marized the ethical point in the design phase in the perspective of relevant regulations of clinical waste sample man-agement and biological sample management. It also analyzed the focus problems including the difference in sample library and clinical laboratory remaining sample as well as the ownership of the sample, to provide theoretical basis for ethics committee to review this kind of protocols.
6.The Inhibiting Effects of Losartan on Proliferation of Cultured Arterial Smooth Muscle Cell and Its Relationship with Neuropeptide Y
Cong GAO ; Jiankang LIU ; Shaohua HUANG ; Minsheng CHEN
Journal of Sun Yat-sen University(Medical Sciences) 2001;22(1):44-47
【Objective】 To explore the mechanism of action of Losa rtan on vascular remodelling in hypertension and its relationship with neuroendo crine factor and renin-angiotensin system.【Methods】 The study consisted of co ntrol group and other three treatment groups: Losartan group、NPY group、and Los artan+NPY group. More than 200 cells were scanned in each group. The methods of c ellular culture, biochemistry and quantitative immunocytochemistry through ACAS5 70 were applied to investigate the proliferation of vascular smooth muscle cell (VSMC) and the expression of proliferating cell nuclear antigen (PCNA) in cultur ed rat VSMC treated with Losartan and Neuropeptide Y (NPY) stimulation. 【Result s】 VSMC proliferation (by absorbauce) in the control group and other three exam ed groups: Losartan group、NPY group and Losartan+NPY group were 0.223 9±0.00 1 0、0.204 5±0.001 3、0.262 6±0.002 5、0.244 0±0.001 3, and PCNA (by fl uorescence intensity) were 1 543±200、1 339±233、1 649±233、1 545±256. It wa s observed that losartan could inhibit the VSMC proliferation in vitro cultu re with and without NPY simulation. Compared with the control groups, the VSMC p roliferation activity and expression of PCNA were obviously descreased in the lo sartan treated gro ups. 【Conclusion】 The results demonstrate that losartan has the inhibitive eff ects on VSMC profiferation and PCNA expression. The results also suggest that lo sartan has anti-NPY effect on VSMC in vascular remodelling of hypertensive vess els.
7.Effect of neuropeptide Y on bcl- 2, bax, fas expressions and proliferation in vascular smooth muscl cells
Cong GAO ; Minsheng CHEN ; Shaohua HUANG ; Jiankang LIU
Chinese Journal of Pathophysiology 2000;16(12):1307-1309
AIM: To explore the effect of neuropeptide Y on expression of apoptosis associated genes and proliferation in vascular smooth muscle cells(VSMC). METHODS: The proliferation activity of VSMC was dterminded by MTr colorimetry. The average fluorescence intensity that represented VSMC nuclear antigen (PCNA) and bcl -2, bax, fas expressions was quantitatively measured by fluorescence immunohistoehemistry. RESULTS: Compared with control, the expressions of bcl - 2, bax, fas, PCNA and the VSMC proliferation activity in VSMC treated with NPY were significantly increased. CONCLUSION: NPY may increase the expression of apoptosis associated genes in VMSC and promote its proliferation.
8.Effect of neuropeptide Y on bcl-2, bax, fas expressions and proliferation in vascular smooth muscl cells
Cong GAO ; Minsheng CHEN ; Shaohua HUANG ; Jiankang LIU
Chinese Journal of Pathophysiology 2000;0(12):-
AIM:To explore the effect of neuropeptide Y on expression of apoptosis associated genes and proliferation in vascular smooth muscle cells(VSMC). METHODS: The proliferation activity of VSMC was dterminded by MTT colorimetry. The average fluorescence intensity that represented VSMC nuclear antigen (PCNA) and bcl-2, bax, fas expressions was quantitatively measured by fluorescence immunohistochemistry. RESULTS: Compared with control, the expressions of bcl-2, bax, fas, PCNA and the VSMC proliferation activity in VSMC treated with NPY were significantly increased. CONCLUSION:NPY may increase the expression of apoptosis associated genes in VMSC and promote its proliferation.
9.Effects of Ca~(2+) /CaM-dependent calcineurin signaling pathway on cardiomyocytes hypertrophy of rats induced by neuropeptide Y
Qi DONG ; Minsheng CHEN ; Shaohua HUANG ; Xiaoyun LI ; Yinghui LI ; Shu ZHANG ; Minsheng CHEN ; Shaohua HUANG ; Xiaoyun LI ; Yinghui LI ; Shu ZHANG ; Zhenxiu LIU ;
Chinese Journal of Clinical Pharmacology and Therapeutics 2000;0(01):-
AIM : To investigate the effects of Ca 2+ /CaM dependent calcineurin(CaN) signaling pathway on cardiomyocytes hypertrophy of rat induced by neuropeptide Y(NPY). METHODS : Cardiomyocytes of neonatal Wistar rats were cultured with NPY of various concentrations (10,100 nmol?L -1 ). Cyclosporine A (CsA) was used to inhibit the activity of CaN. The methods of 3H Leu incorporation was used to assess protein synthesis rate in cardiomyocytes. Western blot and histochemistry were used to measure CaN protein expression and CaN activity in cardiomyocytes. RESULTS : 3 H Leu incorporation of cardiomyocytes were increased significantly by 100 nmol?L -1 NPY ( P
10.Inhibitory effects of antisense oligonucleotides targeting connective tissue growth factor mRNA on the proliferation and collagen synthesis of cardiac fibroblasts
Minsheng CHEN ; Caiwen OU ; Lijian ZHANG ; Qicai LIU ; Shiming LIU ; Shaohua HUANG
Chinese Journal of Pathophysiology 1986;0(02):-
AIM: To observe the effect of AngⅡ on the ex pression of connective tissue growth factor (CTGF) in cultured cardiac fibroblas t (CFs), the antisense oligonucleotides (ASOND) was used to investigate whether CTGF is necessary for the proliferation and collagen synthesis of CFs. METHODS: CFs of SD rats were isolated and cultured. The proliferation and collagen synthesis of CFs were a ssessed by MTT assay and measuring hydroxyproline, respectively. The expression of CTGF mRNA and protein were detected by reverse-transcription PCR (RT-PCR) and Western blotting, respectively. RESULTS: AngⅡ could significantly increase the expression of CT GF both at mRNA and protein level in a dose and time-dependent manner (P0.05). CONCLUSION: It indicates that CTGF is involved in the process of myocardial fibrosis induced by AngⅡ, which may be a target for the treatment o f cardiac fibrosis.