OBJECTIVETo study the effect of taurine on apoptosis in PASMCs, and whether the death-receptor pathway act in the mechanism.

METHODCulture the PASMCs, and divided the cells into control, SD. Acridine orange(AO) assay and western-blot analysis on the expression of Bax, Bcl-2, Procaspase-3 and Fas were used to study the mechanism.

RESULTA major finding of this study is that the Tau effects many apoptosis index, such as increasing the expression of Bax and Fas, decreasing the expression of Procaspase-3, and Bcl-2, accrescencing the mitochondrial depolarization, causing the nuclear shrinkage, all these datas demonstrated that Tau induced the apoptosis in pulmonary artery smooth muscle cells through mitochondrial-dependent pathway.

CONCLUSIONTau induces the apoptosis in pulmonary artery smooth muscle cells through death-receptor.

Animals ; Apoptosis ; drug effects ; Male ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; drug effects ; Pulmonary Artery ; cytology ; drug effects ; Rats ; Rats, Wistar ; Taurine ; pharmacology

OBJECTIVETo study the kinetogenic effects of serum containing Semen Arecae, Dandelion, Semen raphani and Atractylodes macrocephala on the colonic smooth muscle cells of rats.

METHODSSerum containing Chinese materia medicas was made according to standard methods. Smooth muscle cells were isolated from the muscle layers of Wistar rat's colon, referred to modified Bitar's method. The contractile response of colonic smooth muscle cells to serum containing Chinese materia medicas (10%, 50%, 100% concentration) and other medicines (blank and 1 x 10(-3) mol/L acetylcholine) were separately observed. The contractility was presented by the decrease of the cell length between the drug groups and the control.

RESULTSSerum containing each Chinese materia medica can make dose-dependent contraction at different concentrations (P < 0.05), but the strongest effect of each serum had no significant difference (P > 0.05).

CONCLUSIONSerum containing Semen Arecae, Dandelion, Semen raphani and Atractylodes macrocephala can make notable contraction on colonic smooth muscle cells in rats.

Animals ; Cells, Cultured ; Colon ; cytology ; Drugs, Chinese Herbal ; pharmacology ; Medicine, Chinese Traditional ; Muscle Contraction ; drug effects ; Muscle, Smooth ; cytology ; Myocytes, Smooth Muscle ; drug effects ; Rats

OBJECTIVETo study the action mechanism of tetramethylpyrazine (TMP) on the proliferation of vascular smooth muscle cells (VSMCs), thus providing experimental evidence for Chinese medicine to effectively prevent restenosis.

METHODSRats' thoracic aorta VSMCs in vitro cultured (cell line A7r5) were divided into five groups, i.e., the negative control group, the angiotensin II (Ang II, 10(-6) mol/L) group, the low dose TMP (20 micromol/L) plus Ang II group, the middle dose TMP (40 micromol/L) plus Ang II group, the high dose TMP (80 micromol/L) plus Ang II group. The proliferation ratio was detected by MTT. Gene and protein expressions of Wnt4, Dvl-1, beta-catenin, CyclinD1, and collagen I and III were detected with real-time fluorescent quantitative PCR and Western blot respectively.

RESULTSCompared with the negative control group, the proliferation ratio of VSMCs obviously increased in the Ang II group (P < 0.05). Compared with the Ang II group, the proliferation ratio of VSMCs obviously decreased in the middle dose TMP plus Ang II group and the high dose TMP plus Ang II group (P < 0.05). Compared with the negative control group, gene and protein expressions of Wnt4, Dvl-1, beta-catenin, CyclinD1, Col I, and Col III were obviously up-regulated in the Ang II group (P < 0.05). Compared with the Ang II group, mRNA and protein expressions of Wnt4, Dvl-1, beta-catenin, CyclinD1, Col I, and Col III were obviously down-regulated in the middle dose TMP plus Ang II group and the high dose TMP plus Ang II group (P < 0.05). The aforesaid indices were dose-dependent in the low, middle, and high dose TMP plus Ang II groups.

CONCLUSIONTMP inhibited Ang II induced proliferation and collagen secretion of VSMCs through down-regulating Wnt signal pathway.

Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen ; biosynthesis ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; metabolism ; Pyrazines ; pharmacology ; RNA, Messenger ; genetics ; Rats

Benzimidazoles ; pharmacology ; Benzoates ; pharmacology ; Cell Proliferation ; drug effects ; Humans ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Tetrazoles ; pharmacology ; Valine ; analogs & derivatives

Animals ; Cell Proliferation ; drug effects ; Female ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tamoxifen ; analogs & derivatives ; pharmacology

AIMTo investigate the impact of human urotensin II (hUII) on pulmonary arterial smooth muscle cell (PASMCs) cycle in vitro.

METHODSPASMCs dissected from Wistar rats were cultured in vitro, and incubated with series of concentrations of hUII (10(-7) mol/L, 10(-8) mol/L, 10(-9) mol/L) for 12 hours under normoxia or hypoxia condition, in order to analyze cell cycle progression and sub-G1 of PASMCs by using flow cytometric analysis stain of propidium iodide, which represented the proliferative and apoptotic changes in PASMCs.

RESULTSThe study showed a dose-dependent effect of hUII on PASMCs proliferation, which reflected the increase both in percentage of S phase of cell cycle and proliferative index (PI). The response of PASMCs to hUII was different under normoxic and hypoxic conditions. Compared with the control group, the treatment of 10(-7) mol/L, 10(-8) mol/L and 10(-9) mol/L hUII produced an increase of 175%, 136% and 118% under normoxia, respectively, and 135%, 118% and 103% under hypoxia, respectively. The concentration 10(-7) mol/L hUII played a significant role in PASMCs proliferation both under hypoxia and normoxia (P < 0.01). The results of cell cycle did not show sub-G1 of PASMCs at various concentrations of hUII.

CONCLUSIONhUII may stimulate DNA synthesis in S phase cell cycle of PASMCs and the proliferation of PASMCs under normoxia and hypoxia conditions, which promote cell growth in a dose-dependent manner.

Animals ; Cell Cycle ; drug effects ; Cells, Cultured ; Humans ; Male ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Pulmonary Artery ; cytology ; Rats ; Rats, Wistar ; Urotensins ; pharmacology

AIMTo investigate the effect of fractalkine on cell proliferation of cultured rat pulmonary artery smooth muscle cells (PASMCs) in vitro.

METHODSRat PASMCs were cultured in vitro, and treated with different concentrations (10(-10), 10(-9), 10(-8) mol/L) of fractalkine for 12 h, 24 h and 48 h. The cell proliferation was quantified by MTT assay. The cell cycle of PASMCs was measured by flow cytometric(FCM) analysis.

RESULTSMTT assay showed that fractalkine promoted significantly the proliferation of PASMCs, and the effect was concentration-dependent. FCM analysis indicated that fractalkine increased the percentage of S phase and proliferative index (PI). The percentage of S phase and PI of PASMCs were increased after treated with fractalkine for 12 hours, which reached a maximal level at 24 hours.

CONCLUSIONFractalkine promotes rat PASMCs proliferation in a concentration-dependent manner.

Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Chemokine CX3CL1 ; pharmacology ; Male ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Pulmonary Artery ; cytology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the effect of extracted liquid from Qianlietongyu on the proliferation or apoptosis on prostatic smooth muscle cells in vitro.

METHODSAfter extracted liquid from Qianlietongyu treated the cultured prostatic smooth muscle cells, the anti proliferative and apoptotic indices were assessed by MTT assy and terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) respectively.

RESULTSThere was a significant dose-effect relationship between the concentration of extracted liquid from Qianlietongyu and the antiproliferative index on prostatic smooth muscle cells in vitro (P < 0.01), but there was no markedly difference in the apoptosis index between the group of extracted liquid from Qianlietongyu and control group ( P > 0.05).

CONCLUSIONExtracted liquid from Qianlietongyu may show significant antiproliferative effect on prostatic smooth muscle cells in vitro, without inducing apoptosis.

Apoptosis ; Cell Proliferation ; Cells, Cultured ; Humans ; Male ; Myocytes, Smooth Muscle ; drug effects ; Plant Extracts ; pharmacology ; Prostate ; cytology ; drug effects

Calcium channels exist extensively in the membrane of cardiac, skeletal, smooth muscle cell and neuron. Calcium channel blockers (CCB) were widely used for the treatment of cardiovascular diseases because they could relax vascular smooth muscle. Experimental researches on calcium channel blockers relaxing corpus cavernosum smooth muscle have been reported recently. Whether the blockers can be used for the clinical diagnosis and treatment of erectile dysfunction still need to be further investigated.
Animals ; Calcium Channel Blockers ; pharmacology ; therapeutic use ; Calcium Channels ; metabolism ; Cardiovascular Diseases ; drug therapy ; Humans ; Male ; Muscle Relaxation ; drug effects ; Muscle, Smooth, Vascular ; drug effects ; Myocytes, Smooth Muscle ; drug effects ; Penile Erection ; drug effects

OBJECTIVETo investigate the effects of 17β-estrogen on expressions of C-reactive protein (CRP) and its mRNA in vascular smooth muscle cells(VSMCs).

METHODSImmunocytochemistry was used to detect CRP level in normal VSMCs. The expressions of C-reactive protein and p-ERK1/2 in Ang-II-stimulated VSMCs were evaluated with Western blot. C-reactive protein mRNA was examined with RT-PCR.

RESULTS17β-estrogen had no effect on cell morphology and C-reactive protein expression in normal VSMCs; however, C-reactive protein and mRNA, as well as p-ERK1/2 were decreased in Ang-II-stimulated VSMCs after 17β-estrogen treatment in a concentration-dependent manner.

CONCLUSION17β-estrogen may inhibit the expression of C-reactive protein and its mRNA in Ang-II-stimulated VSMCs via ERK1/2 signal transduction pathway in a concentration-dependent way.

Animals ; C-Reactive Protein ; genetics ; metabolism ; Cells, Cultured ; Estrogens ; pharmacology ; Male ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; drug effects ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley