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Objective:To investigate the therapeutic effect of montelukast sodium combined with tiotropium bromide in the treatment of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and its effect on serum tumor necrosis factor like weak apoptosis inducing factor (TWEAK), monocyte chemoattractant protein-1 (MCP-1) and inflammatory factor.Methods:From January 2019 to January 2020, 102 patients with AECOPD were selected from Kecheng Xiangyuan Hospital of Traditional Chinese Medicine of Quzhou.According to the method of random table, they were divided into observation group and control group, with 51 cases in each group.The observation group was treated with montelukast sodium tablets combined with tiotropium bromide, while the control group was treated with tiotropium bromide.The course of treatment in both two groups was 2 weeks.The therapeutic effect, lung function and blood gas analysis, TWEAK, MCP-1 and inflammatory factors were compared before and after treatment.Results:The total effective rate of the observation group (92.16%, 47/51) was higher than that of the control group (72.55%, 37/51) (χ 2=6.746, P<0.05). After treatment, the PEF[(2.98±0.21)L/s], FEV 1[(2.13±0.15)L] and PaO 2[(87.81±6.31)mmHg] in the observation group were higher than those in the control group[(2.43±0.35)L/s, (1.76±0.23)L and (74.39±5.48)mmHg], while PaCO 2[(36.28±4.15)mmHg] was lower than that in the control group[(49.83±4.26)mmHg], the differences were statistically significant ( t=9.623, 9.620, 11.467, 16.271, all P<0.05). The serum levels of TWEAK[(0.46±0.07)pg/L] and MCP-1[(93.42±13.27)ng/L] in the observation group were lower than those in the control group[(0.58±0.06)pg/L and (115.63±18.43)ng/L]( t=9.295, 6.984, all P<0.05). The levels of IL-13[(94.56±13.24)ng/L], IL-18[(43.87±3.89)ng/L] and TNF-α[(131.29±15.36)ng/L] in the observation group were lower than those in the control group[(113.21±15.53)ng/L, (56.78±4.25)ng/L and (131.29±15.36)ng/L]( t=6.526, 15.941, 8.726, all P<0.05). Conclusion:Montelukast sodium combined with tiotropium bromide is effective in the treatment of AECOPD.It can reduce the levels of serum TWEAK and MCP-1, and reduce the inflammatory response.
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Objective The study is to investigate the role of miR-328 in endothelial mesenchymal transition (EMT)induced by high glucose in human umbilical vein endothelial cells (HUVECs)and its signaling mechanism.Methods HUVECs were cultured in high glucose environment to induce EMT;The recombinant lentiviruses were created by miR-328 and antagomiR- 328 transfection of HUVECs.The experiment was divided into seven groups: normal glucose;mannitol group;high glucose;miR-328;miR-328 virus negative control;high glucose + U0126;miR-328 + U0126.Double immunofluorescent staining was used to determine expression of EMT markers;Changes in miR-328 expression is examined by RT-qPCR;The expressions of type Ⅰ/Ⅲ collagen,p-MEK1/2 and p-ERK1/2 are examined by Western blot.Results 1)HUVECs showed positive staining for CD31 and α-SMA in high glucose group.2)The expression of miR-328 was up-regulated(P<0.05)in HUVECs treated by high glucose or miR-328.Compared with high glucose group or miR-328 group,miR-328 expression was less pronounced aftertreatment with U0126.3)The expressions of type Ⅰ/Ⅲ collagen increased in HUVECs treated by high glucose or miR-328(P<0.05) Compared with high glucose group or miR-328 group,typeⅠ/Ⅲ collagen expressions were less pronounced after treatment with U0126.4)The expressions of p-MEK1/2 and p-ERK1/2 were increased in HUVECs treated by high glucose or miR-328 in comparison to the control group (P<0.05);a lower expression of p-MEK1/2 and p-ERK1/2 were observed in U0126 group than in high glucose group or miR-328 group.Conclusions The phenomenon of EMT in HUVECs is induced by high glucose with increased expression of miR-328;overexpression of miR-328 induced EMT in HUVECs;miR-328 induced EMT is related with MEK1/2-ERK1/2 signaling pathway.
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Objective To investigate the effect of 5-azacytidine(5-AZA) on apoptosis of bone marrow mesenchymal stem cells(BMSCs).Methods BMSCs were isolated from bone marrow of mouse tibia and femur; the expression of MSC specific markers CD44 and CD90 in BMSCs was measured by immunofluorescence staining;BMSCs were cultured in vitro in the medium supplemented with 0,10 and 20 μmol/L 5-AZA for 48 hours.Cell apoptosis was measured with fluorescent labeled inhibitor of caspases (FLICA) apoptosis kit and 4',6-diamidino-2-phenylindole (DAPI) staining ;the expression of apoptosis-related proteins Annexin V and Caspase-3 in the treated BMSCs was detected by Western blot.Results In this study,BMSCs positively expressed MSC specific markers CD44 and CD90.DAPI staining and Caspase-3 staining both showed that 10 and 20 μmol/L 5-AZA markedly increased apoptotic rate of BMSCs;the apoptosis-positive rate in DAPI staining was (21.086 ± 2.601) ％,(34.467 ± 3.724) ％ and (46.512 ± 3.864) ％,the apoptosis-positive rate in Caspase-3 staining was (5.354 ± 0.735)％,(15.462 ± 2.385)％ and (28.190 ± 4.190)％ in the controls,10 and 20 μmol/L 5-AZA groups,and there were significant differences among the control group and 5-AZA treated groups(all P ＜0.01).Western blot assay showed that Annexin V and Caspase-3 were both markedly upregulated in 5-AZA treated cells;the relative level of Annexin V expression was(26.612 ±2.184)％,(42.873 ±4.313)％ and (50.056 ± 4.457) ％,the relative level of Caspase-3 expression was (19.231 ± 2.683) ％,(38.618 ± 5.385) ％ and(91.235 ± 7.116)％ in the controls,10 and 20 μmol/L 5-AZA groups,and there were significant differences among the control group and 5-AZA treated groups (all P ＜ 0.01).Conclusion The commonly used doses of 5-AZA can induce apoptosis of BMSCs.
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Objective To research the mechanism or pathway through which Substance P(SP) inhibits r-aminobutyric acid(GABA) activated currents in bullfrog dorsal root ganglion(DRG) neurons.Method The experiment was conducted on freshly isolated bullfrog dorsal root ganglion neurons using a whole-cell patch-clamp technique.Results SP could caused a slow inward current when SP was applied to DRG neurons;SP could inhibits GABA-activated currents;The inhibition could be reduced largely when protein kinase C(PKC) inhibiter,1-(5-isoquinolinesulphorry)-2-methylpiperazine(H-7), was dialyzed in cell body.Conclusion The SP ton inhibit GABA-activated currents through protein kinase C.
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Object It was reported that salvianolic acid A from Salvia miltiorrhiza Bge could improve memory dysfunction of mice with cerebral ischemia reperfusion injury The effects of total salvianolic acids (Sal), including salvianolic acid A and B, rosmaric acid and protocatechic aldehyde was now studied to observe its effect on cerebral ischemia reperfusion injury in hope of obtaining a preliminary view on its mechanism of action Methods The effects of Sal on lactic dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) of cerebral ischemia reperfusion injured mouse and rat models were observed Results Sal 10, 20 mg/kg iv and 5, 10 mg/kg iv could markedly increase the activities of LDH and SOD and lower the production of MDA in the injured cerebral tissue On focal cerebral ischemia reperfusion injured rat, 24 h reperfusion after 2 h ischemic injury, 5, 10 mg/kg iv Sal could decrease infarct size, ameliorate neurological deficit with obvious inhibition of the decrease of LDH and SOD activities and the over production of MDA Conclusion Sal showed obvious protective effects on cerebral ischemia reperfusion injuries of mice and rats via attenuating oxygen free radical
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AIM To study the effect and mechanism of sildenafil on rabbit corpus cavernosum in vitro . METHOD Rabbit corpus cavernosum(RCC) segments were incubated with various concentrations of sildenafil. The formation of cGMP was stimulated with 1 ?mol?L -1 sodium nitroprusside(SNP), and the cyclic GMP concentration was measured by radioimmunoassy technology. In the organ bath, strips of RCC were precontracted with 10 ?mol?L -1 phenylephrine. Sildenafil were added with increasing doses gradually, graded relaxations were induced using various concentrations of sodium nitroprusside (SNP) and methacholine (MCH). RESULT In the presence of SNP, the cGMP concentration was increased in rabbit penile tissue, the increase of cGMP was greater when sildenafil was added. Sildenafil 10、100 nmol L -1 、1 ?mol?L -1 dose-dependently relaxed RCC strips. CONCLUSION Sildenafil increases cGMP concentration in RCC is attributed to the augmentation of NO/cGMP pathway, and the accumulation of cGMP improves the relaxation of RCC.