Objective To investigate the expression changes of stromal interaction molecule 1 (STIM1) in vascular smooth muscle cells in balloon injury of carotid artery in rat in order to explore the proliferation mechanism of vascular smooth muscle cells. Methods A rat model of vascular restenosis induced by injury to the carotid arteries due to balloon dilatation was reproduced in present study. A total of 18 SD rats were randomly divided into 3 groups (6 each): control group, 7-day group and 14-day group after balloon injury to the carotid artery. The expression of STIM1 mRNA in vascular smooth muscle cells was assayed with reverse transcription polymerase chain reaction (RT-PCR), and the STIM1 protein was assessed by immunohistochemistry. The histopathology of the arteries was examined after by HE staining. Results Intima area/media area ratio (IA/MA) was significantly increased in 7-day group after balloon injury than in control group (P

Objective To investigate the effects of B-type natriuretic peptides (BNP) on expression of monocyte chemoattractant protein-1(MCP-1) in rat peritoneal macrophages and to identify the inflammation-mediated effects of BNP in macrophages. Methods Peritoneal macrophages of primary culture were treated with BNP, BNP+HS-142-1, or BNP+TNF-?+HS-142-1. The protein expression of MCP-1 was measured by Western blot. Results BNP enhanced the MCP-1 protein expression in macrophages, and this effect could be abrogated by HS-142-1. In addition, BNP could inhibit TNF-? induced MCP-1 expression. Conclusion BNP can induce the MCP-1 protein expression in macrophages, suggesting BNP has a pro-inflammatory effect. However, BNP also can inhibit TNF-? induced MCP-1. These findings suggest that the effect of inflammation-mediated by BNP is biphasic though the mechanism is still unclear.

Objective To explore the mechanism by which urotensin Ⅱ induces hypertrophy of the cultured rat cardiomyocytes. Methods The cultured cardiomyocytes from neonatal SD rats were treated with urotensin Ⅱ, also with cyclosporine A for its blocking effect on urotensin Ⅱ induced cardiomyocytes hypertrophy. The mRNA and protein levels of ?-MHC and CaN were evaluated by real-time PCR and Western blotting, respectively. Results In the cells treated with 10-8 and 10-7 mol/L urotensin Ⅱ, the mRNA and protein levels of ?-MHC and CaN were significantly higher than that of control (P

Objective To investigate the effect of all-trans retinoic acid (at-RA) on fetal alveolar epithelial type Ⅱ cells (fAEC Ⅱ s) proliferation and the expression of pulmonary surfactant C (SPC) as well as aquaporin 5 (AQP5).Methods fAEC Ⅱ s were isolated and purified from fetal lung of pregnant SD rats (19 days).After being cultured for 1 day,and the fAEC Ⅱ s were interfered by at-RA for 1,2 and 3 days.Cell proliferation,viability as well as growth state,expressions of SPC mRNA as well as AQP5 mRNA and expressions of protein SPC as well as AQP5 were respectively detected by using 4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT),inverted microscope,real-time fluorescence quantitative PCR (RT-PCR) and Western blot.Results (1) When fAEC Ⅱ s were treated with at-RA for 1 day,and the cell proliferation and viability did not change (P ＞ 0.05),while the proliferation and viability were significantly improved in 2 days (P ＜ 0.05),and the difference was the most obvious (P ＜ 0.05) at 3 days.(2)Compared with the control group,the cell growth state was better,and the cell adherence was tighter and the refraction was higher in at-RA group.(3) Compared with the control group,at-RA up-regulated the expressions of AQP5 mRNA and AQP5 protein(t =-19.58,-10.44,-16.01,-46.25,-12.79,-27.96,all P ＜ 0.05),and the percentages of control group were 281.07％,766.67％,1 163.33％ and 792.65％,1 310.52％,1 561.56％ in 1,2 and 3 days respectively.(4) Compared with control group,the expressions of SP-C mRNA and SPC protein were up regulated when cells were exposed to at-RA for 1 and 3 d,but while they were down-regulated at 2 days(protein:the percentages of control group were 615.480％,369.450％ and 11.269％,respectively ; mRNA:728.33 ％,400.83 ％,66.57％,respectively)(t=-26.34,-25.26,13.80,-25.25,-31.71,9.12,all P＜0.05).Conclusions at-RA can promote the proliferation and differentiation of fAEC Ⅱs,enhance the fAEC Ⅱ s viability,and improve the expression of SPC and AQP5.

Objective To study the effects of the Notch ligands Dlk1 and recombinant human nucleu factorκB (Jagged1) on the proliferation and transdifferentiation of the type Ⅱ alveolar epithelial cells when the Notch signaling pathway activated.Methods The primary type Ⅱ alveolar epithelial cells (AEC Ⅱ) cultured with recombinant protein Dlk1 and recombinant human nucleu factor-κB (rhNF-κB) (activator of Jagged1),respectively,and then cultured with DMEM (containing 120 mL/L FBS) as controls.Proliferation and differentiation conditions of the AEC Ⅱ were observed at 48 h,72 h,96 h time point by the light microscope and electron microscopes separately.Cell number was counted with hemacytometer; the proliferation rate was measured by methyl thiazolyl tetrazolium (MTT) ; Immunofluorescence double standard method was used to detect the AEC Ⅱ specific surfactant protein C (SP-C) and AEC Ⅰ specific protein aquaporin5 (AQPS) ;the expression of SP-C,AQPS,Dlk1,Jagged1,Notch1 and Hes1 mRNA were detected by real time-PCR.Results The cell population and proliferation:compared with control group,AEC Ⅱ proliferation was promoted in the Dlk1 group [cell numbers (× 109/L) 9.05 ± 0.45 vs 7.95 ± 0.65,11.68 ± 0.43 vs 8.68 ± 0.52,11.55 ± 0.17 vs 8.73 ± 0.48,all P ＜ 0.05 ; MTT results (value A) 0.699 ± 0.050 vs 0.462 ± 0.080,0.912 ± 0.080 vs 0.535 ±0.040,0.726 ±0.050 vs 0.540 ±0.020,all P ＜0.05] and decelerated AEC Ⅱ transdifferentiation into AEC Ⅰ ; while AEC Ⅱ proliferation was inhibited in rhNF-κB group [cell numbers (× 109/L) 4.95 ± 0.33 vs 7.95 ± 0.65,4.73 ±0.71 vs 8.68 ± 0.52,4.04 ± 0.11 vs 8.73 ± 0.48,all P ＜ 0.05; MTT results (value A) 0.398 ± 0.030 vs 0.462 ± 0.080,0.402 ± 0.070 vs 0.535 ± 0.040,0.380 ± 0.110 vs 0.540 ± 0.020,all P ＜ 0.05] and accelerated AEC Ⅱ transdifferentiation into AEC Ⅰ.One-Way ANOVA showed that the difference among the 3 groups had statistical significance (cell numbers:F =486.73,P =0.02; cell proliferation:F =37.16,P =0.02).The mRNA expression:compared with control group,the expression of SP-C mRNA of Dlk1 group was significantly higher (P ＜ 0.05) while the expression of AQP5 mRNA was remarkably lower and delayed (P ＜ 0.05),the expression of Jagged1 mRNA was weak or little,Dlk1 and Notch1 mRNA were up-regulated (P ＜ 0.05),and the Hes1 mRNA was reduced (P ＜ 0.05) ; the expression of SP-C mRNA of rhNF-κB group was significantly reduced (P ＜ 0.05),while the AQP5 mRNA expressed ahead of time and increased (P ＜ 0.05),Jagged1,Hes1 and Notch1 mRNA were higher (P ＜ 0.05),and the Dlk1 mRNA was weak.One-Way ANOVA showed that the difference in the expressions of SP-C,AQP5,D1k1,Jagged1,Hes1 and Notch1 mRNA among the 3 groups had staistical significance (F =96.80,P =0.01 ; F =82.55,P =0.01 ; F =269.80,P=0.00;F =312.34,P =0.00;F =169.17,P =0.01;F =19.85,P =0.02).Conclusions There are varied effects on proliferation and differentiation of the AEC Ⅱ when the Notch signaling is activated by different ligands:Dlk1 promoted proliferation and inhibited differentiation,while Jagged1 inhibited proliferation and promoted transdifferentiation.

This article reported the comprehensive management of an extremely preterm infant with severe bronchopulmonary dysplasia. The patient born at 26 +6 gestational weeks was transferred to Children's Hospital of Fudan University due to invasive mechanical ventilation dependence at 61 d after birth and was diagnosed with severe bronchopulmonary dysplasia. A comprehensive treatment plan was adopted, including appropriate fluid restriction, improving nutrition, glucocorticoid administration, using antibiotics against Ureaplasma urealyticum infection to reduce pulmonary parenchymal lesions and alleviating pulmonary hypertension. The preterm infant was successfully extubated to non-invasive ventilation and subsequently weaned to a high-flow nasal cannula. Then, the patient was discharged at 372 d after birth (correct gestational age nine months and six days). At the 3-month follow-up after discharge, the patient remained on high-flow oxygen, but with lower flow and concentration of oxygen. Moreover, the growth, development and lung images were significantly improved. Follow-up to correct gestational age one year and 11 months, the child was not on oxygen any more, but on rehabilitation due to language and motor development retardation.

AIM: To investigate the pharmacokinetic properties of the main active components of Dalitong extract in SD rats after oral administration using UPLC-MS / MS. METHODS: An UPLC-MS / MS method was established to simultaneously detect tetrahydropalmatine, nobiletin and costunolide in the plasma and tissues of SD rats. The method was applied to investigate the pharmacokinetic characteristics and tissue distribution. RESULTS: After a single oral administration, the three active components were rapidly absorbed into the body, with a peak concentration (Cmax) of (13.73 ± 7.50), (27.01 ± 17.69) and (6.73 ± 29.94) ng / mL for tetrahydropalmatine, nobiletin, and costunolide, respectively. The time to reach the peak concentration (Tmax) was (1.40 ± 0.93), (0.63 ± 0.28) and (2.38 ± 8.81) h, respectively. The area under the curve (AUC) was (80.43±40.03), (41.30±28.69) and (303.90 ± 136.69) ng · h · mL