OBJECTIVETo investigate the contribution of mitochondrial pathway in the apoptosis induced by puerarin (PUE) in pulmonary artery smooth muscle cells.

METHODCultured rat pulmonary artery smooth muscle cells (PASMC) were intervened by high, middle and low dose of puerarin (1.5 x 10(-3), 1.5 x 10(-4), 1.5 x 10(-5) mol x L(-1)). The change of mitochondrial membrane potential was observed. Western blot detected the expression of apoptosis-related gene Caspase-9, Bax and Bcl-2 protein.

RESULTCompared with the control group, mitochondrial membrane potential significantly decreased in puerarin groups. Puerarin can enhance the expression of Caspase-9 and Bax protein, decrease the expression of Bcl-2 protein. Puerarin also has a concentration-dependent on the induction of PASMC.

CONCLUSIONPuerarin can induce PASMC apoptosis through mitochondrial pathway.

Animals ; Apoptosis ; drug effects ; Caspase 9 ; metabolism ; Cells, Cultured ; Isoflavones ; pharmacology ; Male ; Mitochondria ; drug effects ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; drug effects ; physiology ; Proto-Oncogene Proteins c-bcl-2 ; analysis ; Pulmonary Artery ; cytology ; drug effects ; Rats ; Rats, Wistar

Microtubule inhibitor has been a hot area of anticancer drugs research.Microtubule inhibitor exert an anti-tumor effect by promoting or inhibiting the microtubule aggregation to break the dynamic balance of microtubule,hindering the spindle forma-tion of tumor cells,and then blocking the process of cell divi-sion.Mitotic catastrophe is a cell death phenomenon that is caused by abnormal cell division and damage of spindle structure in cell mitosis phase.In recent years more and more attention has been paid to mitotic catastrophe cell death because it has
been confirmed clinically that microtubule inhibitors can induce mitotic catastrophe death of tumor cells.This paper reviews the latest research progress of microtubule inhibitors,and discusses the molecular mechanisms of mitotic catastrophe cell death tumor cells induced by microtubule inhibitors.

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

Objective:To investigate the effect of milking diary combined with syringe collection of colostrum on early lactation.Methods:Totally 80 cases of separated mothers and infants hospitalized in the maternity ward of our hospital from February to November 2018 were selected as research objects, February to June as control group, July to November as experimental group, 40 cases respectively, two groups were given routine maternal lactation, experimental group in regular maternal lactation guidance, on the basis of guiding diary records milking and provides the syringe collection of colostrum. Comparison of two groups of maternal postpartum 3 days milking frequency and milking, lactation, start time, lactation Ⅱ period time, breast tenderness and 42 days exclusive breastfeeding rates.Results:Postpartum 24 hours, 48 hours, 72 hours of milking times of delivery woman in experimental group were respectively (7.25 ± 1.53), (7.40±1.26), (8.50±0.82) times, which were higher than (4.18 ± 2.62), (6.35±1.73), (7.35±1.72) times in control group, the difference was statistically significant ( t values were -6.408, -3.102, -3.824, P < 0.01). Milking 49-72 hours was 50.30 ml, which was significantly higher than 30.70 ml of control group, the difference was statistically significant ( Z value was 3.773, P < 0.01); mammary start time, lactation Ⅱ period significantly ahead of time, respectively (9.82 ± 3.62) hours in advance, and (15.83 ±0.78) hours, the difference was statistically significant ( t values were 2.480,4.871, P<0.05); breast pain Ⅲ degrees within 72 hours of experimental group 5.0% (2/40) was significantly lower than the control group 25.0% (10/40), 42 days exclusive breastfeeding rate 62.5% (25/40) was significantly higher than the control group 22.5% (9/40), the differences were statistically significant ( χ2=6.772, 13.095, P<0.05). Conclusion:Joint syringe collection colostrum milk a diary method can effectively improve maternal milk, increase the amount of milk secretion, and early lactation start time and duration of lactation Ⅱ period, so as to promote exclusive breastfeeding rate and duration of breastfeeding, and can effectively reduce the degree of breast tenderness, worthy of clinical popularization and application

OBJECTIVE：To investigate the effects and mechanism of puerarin （Pue） on hypoxia-induced pyroptosis of pulmonary artery smooth muscle cells （PASMCs）. METHODS ：PASMCs of rats as research objects were randomly divided into normoxia group ，hypoxia group and hypoxia+Pue group （0.2 mmol/L）. Except for normoxia group ，other groups were cultured with 5％ CO2 and 3％ O2 at 37 ℃ for 24 hours to establish hypoxia model. Western blot assay was used to detect the expression of pyroptosis related proteins [NOD-like receptor protein- 3 （NLPR3），caspase-1，interleukin-1 β （IL-1 β），apoptosis-associated speck-like protein （ASC）]. Lactate dehydrogenase （LDH）release assay was used to detect the release of LDH in cells ；Hoechst 33342/PI double staining test was adopted to detect the proportion of pyroptosis positive cells. PASMCs was randomly divided into normoxia group+control plasmid group ，hypoxia+control plasmid group ，hypoxia+over-expression plasmid group and hypoxia+ over-expression plasmid+Pue group. Except for the normoxia+control plasmid group ，the other groups were established hypoxia model by the same method. After transfection of control plasmid or NLRP 3 over-expression plasmid ，Western blot ，LDH release test and Hoechst 33342/PI double staining test were used to investigate whether Pue could inhibit hypoxia-induced PASMCs pyroptosis by interfering with the activity of NLRP 3 inflammasomes. RESULTS ：Compared with normoxia group ，the expression of pyroptosis related proteins ，the release of LDH and the proportion of pyroptosis positive cells were increased significantly in hypoxia group （P＜0.05 or P＜0.01）. Pue had the effect of reversing the above indexes （P＜0.05 or P＜0.01）. When the NLRP 3 inflammasome was over-expressed ，the expression of pyroptosis related proteins ，the release of LDH and the proportion of Δ 基金项目：黑龙江省自然科学基金资助项目（No.ZD201416） pyroptosis positive cells were increased significantly （P＜0.05 ＊教授，博士生导师 ，博士。研究方向 ：心血管药理学 。电话： or P＜0.01）. Pue could inhibit the above phenomenon through 0451-58853046。E-mail：zhangxd85@163.com regulating NLRP 3 inflammasome （P＜0.05 or P＜0.01）. 中国药房 2021年第32卷第11期 China Pharmacy 2021Vol. 32 No. 11 ·1337· CONCLUSIONS：Pue can significantly inhibit the hypoxia-induced pyroptosis of PASMCs by down-regulating the expression of pyroptosis related proteins ，reducing the release of LDH and proportion of pyroptosis positive cells. The mechanism is related to the activity inhibition of NLRP 3 inflammasome.