Many cardiovascular diseases, such as pulmonary hypertension, atherosclerotic plaque formation and restenosis after angioplasty, are charaterized by vascular remodeling resulting from migration and proliferation of vascular smooth muscle cells. Integin receptors can activate the expression of related genes through the corresponding signal pathway, and lead to vascular smooth muscle cell' s proliferation and migration and other biological behavioral change, which may be a new hotspot of pathogenesis and intervention of vascular remodeling.

Objective To observe the effect of light emitting diode (LED) red light irradiation on serum lipid in experimental hyperlipidemia rats. Methods 36 healthy male Sprague-Dawley rats were randomly divided into normal control group (n=12) and hyperlipidemic model group (n=24). The normal group was fed with normal diet while the hyperlipidemic model group with fat-rich forage for 6 weeks. The hyperlipidemic model group rats were randomly divided into the hyperlipidemic control group (n=12) and LED treatment group (n=12), and the latter accepted LED red light irradiation for 28 d. The levels of serum lipid including total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL-C), high-density lipoprotein (HDL-C), and the activities of lipoproteinesterase (LPL) and hepatic lipase (HL) were detected with biochemical assay. The expression of 3-hydroxy-3-methylglutaryl coenzyme A reducase (HMG-CR) of hepatic tissue were measured with immunohistochemical staining. Results Compared with the hyperlipidemic control group, the levels of serum TC, TG and LDL-C decreased while the serum HDL-C increased significantly in the LED treatment group (P<0.01) after treated with LED. The levels of LPL and HL in serum increased (P<0.01) while the activity of HMG-CR decreased (P<0.05). Conclusion LED red light irradiation might play a regulating effect on serum lipid by enhancing the activities of LPL and HL and inhibiting the expression of HMG-CR to interfere the metabolism of TC, TG, LDL-C and HDL-C.

Objective To explore the effects of the extracellular regulated protein kinase’s (ERK1/2) inhibitor PD98059 and ino-sitol triphosphate kinase (PI3K/PKB) signaling pathway’s inhibitor LY294002 on extracellular matrix (ECM) deposition in pulmonary arterial smooth muscle cells (PASMCs) stimulated by connective tissue growth factor (CTGF). Methods PASMCs of SD rat were cul-tured in vitro. The PASMCs were divided into control group, CTGF group, CP (CTGF+PD98059) group, CL (CTGF+LY294002) group and CPL (CTGF+PD98059+LY294002) group. Real-time lfuorescent quantitative RT-PCR was used to detect the expression of colla-gen III and ifbronectin mRNA of PASMCs, and the expression of collagenШprotein of PASMCs was detected by immunohistochem-istry and western-blot. Results The expressions of collagenШand ifbronectin mRNA of PASMCs stimulated with CTGF (50 ng/ml) for 48 h were signiifcantly higher than those in control group, and the collagen proteinШof PASMCs was decreased signiifcantly after stimulation with CTGF (50 ng/ml) for 72 h (P<0.05). The expressions of collagenШand ifbronectin mRNA in PASMCs cultured with PD98059 (20μmol/L) and/or LY294002 (10μmol/L) for 48 h was signiifcantly lower than those in CTGF group (P<0.05). The collagen proteinШin PASMCs cultured with PD98059 (20μmol/L) and/or LY294002 (10μmol/L) for 72 h was increased (P<0.05). The expres-sions of collagenШand ifbronectin mRNA of PASMCs stimulated with both PD98059 and LY294002 were more signiifcant. Conclu-sions CTGF may increase the expression of collagenШand ifbronectin mRNA in PASMCs, which may contribute to the deposition of ECM in PASMCs during pulmonary vascular remodeling. PD98059 and LY294002 may repress ERK1/2 and PI3K/PKB signaling pathways and interfere with the biological effect of CTGF.

Objective To explore the mechanisms of integrin β1 on connective tissue growth factor(CTGF)-induced proliferation,migration,change of cytoskeleton of pulmonary arterial smooth muscle cell(PASMC) in vitro,and to investigate the effects of CTGF-integrin β1 signal pathway on pulmonary vascular remodeling in pulmonary arterial hypertension (PAH).Methods Pulmonary artery smooth muscle cells of SD rats were cultured in vitro.WST-1 assay was used to detect the effects of anti-integrin β1 antibody on CTGF-induced proliferation of PASMC.Transwell chambers were used to observe the effects of anti-integrin β1 antibody on CTGF-induced migration of PASMC.The cytoskeletal rearrangement was observed with coomassie brilliant blue R250 staining and Confocal Lasar Scanning Microscopy (CLSM).Results Different concentration of anti-integrin β1 antibody could inhibit the proliferation of PASMC induced by CTGF,which presents concentration dependent pattern (P ＜ 0.05).The higher the concentration of anti-integrin β1 antibody,the more severity the proliferation of PASMC induced by CTGF was inhibited.and inhibition rate of PASMC proliferation was the highest at 72 hours.Anti-integrin β1 antibody(15 mg/L) decreased significantly the number of PASMC passing through Transwell induced by CTGF,compared with CTGF group (P ＜ 0.01).Meanwhile,antiintegrin β1 antibody could change cytoskeletal rearrangement of PASMC induced by CTGF.Conclusions Integrin β1mediates the proliferation,migration,cytoskeletal rearrangement of PASMC induced by CTGF.The CTGF-integrin β1signal pathway may play a key role in proliferation,migration,cytoskeletal rearrangement PASMC.

ObjectiveTo investigate the features of normal and psoriasis skin on ultrasound biomicroscopy (UBM) and explore the method of thickness measurement.MethodsUsing 50 MHz ultrasound probe of biological microscope, ultrasonographic observation and ultrasonic thickness measurement were conducted in 90 normal adults and 40 psoriasis patients. Innormal patients, ultrasound evaluations were performed at 10 different parts of the body skin.ResultsOn sonogram, the normal skin showed a “sandwich” structure with two parallel hyperechoic bands and the middle isoechoic dots and short liens. The sonograms of the psoriasis skin showed obviously thickened epidermis and dermis, disordered internal structure and clear boundary from adjacent normal skin. The range of the epidermis’ thickness measurement was between the medial forearm (0.12±0.03) mm and the palm (0.29±0.15) mm. The range of dermal thickness measurement was between the back hand (1.18±0.32) mm and parasternal (1.55±0.21) mm. Psoriasis skin was thicker than the uninvolved skin (P<0.001). And the dermis’ thickness of uninvolved skin in psoriasis patients was thicker than that of the normal adults (P<0.001).ConclusionNormal adult’s epidermis, dermis and skin appendages can be shown clearly using 50 MHz ultrasound biomicroscopy. And ultrasound biomicroscopy canaccurately measure the thickness of dermis and epidermis, which provides the basis for the diagnosis and treatment of psoriasis.

Objective To explore the 3D gait analysis of stroke hemiplegic patients. Methods 28 stroke hemiplegic patients were examined with the 3D gait analysis system before and after 6-week rehabilitation. Results After rehabilitation, support phase time of the affected lower limb increased and swing phase time decreased (P<0.05). Step length, stride length and walking speed increased (P<0.05). There was significantly difference in range of motion (ROM) of hip deduction/abduction, flexion/extension, and knee flexion/extension, and ankle internal/external rotation, varus/eversion, dorsiflexion/plantar flexion before and after rehabilitation (P<0.05). Conclusion 3D gait analysis system can evaluate the patient's gait objectively and quantitatively, and provide the basis for rehabilitation assessment.

Objective:To investigate the effect of Xidi Liangxue recipe on the proliferation and apoptosis of HaCaT cells through the long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) /microRNA (miR) -485-5p/signal transducer and activator of transcription 3 (STAT3) regulatory network. Methods:HaCaT cells were induced by interleukin-17 (IL-17), and the mRNA and protein expression of lncRNA NEAT1, miR-485-5p and STAT3 was detected in IL-17-induced HaCaT cells and normal human epidermal keratinocytes (NHEK) by quantitative PCR (qPCR) and Western blot analysis, respectively. The location of lncRNA NEAT1 and miR-485-5p in IL-17-induced HaCaT cells was observed by fluorescence in situ hybridization (FISH), and the targeted regulatory relationship among lncRNA NEAT1, miR-485-5p and STAT3 was verified by double-luciferase reporter gene assay. Chinese herbs were decocted according to the Xidi Liangxue recipe, SD rats were divided into two groups to be gavaged with the above decoctions (medicated group) or physiological saline (control group) for 5 days, and then serum samples were collected from the above two groups of rats separately. The IL-17-induced HaCaT cells were divided into 4 groups: control group treated with the control sera, lncRNA-NEAT1 overexpression group transfected with lncRNA-NEAT1 overexpression vectors and treated with the control sera, Xidi Liangxue recipe group treated with the medicated sera, and Xidi Liangxue recipe + lncRNA-NEAT1 overexpression group transfected with lncRNA-NEAT1 overexpression vectors and treated with the medicated sera. qPCR, Western blot analysis, flow cytometry, and cell counting kit (CCK8) assay were performed to determine the mRNA and protein expression of lncRNA NEAT1, miR-485-5p and STAT3, and to evaluate cell proliferation and apoptosis. The two independent samples t-test was used for comparisons between two groups, one-way analysis of variance for comparisons among multiple groups, and least significant difference (LSD) t-test for multiple comparisons. Results:The IL-17-induced HaCaT cell group showed significantly increased relative expression levels of lncRNA NEAT1 and STAT3 mRNA (1.84 ± 0.21, 2.20 ± 0.24, respectively) and significantly increased protein expression of STAT3 and p-STAT3 (1.27 ± 0.13, 2.43 ± 0.16, respectively), but significantly decreased expression level of miR-485-5p (0.32 ± 0.04) compared with the NHEK group (lncRNA NEAT1 and STAT3 mRNA: 1.00 ± 0.11, 1.00 ± 0.11, respectively, both P < 0.05; STAT3 and p-STAT3 protein: 1.00 ± 0.11, 1.00 ± 0.10, t = 2.54, 3.02, respectively, both P < 0.05; miR-485-5p: 1.00 ± 0.12, t = 2.94, P = 0.015). FISH demonstrated that miR-485-5p and lncRNA NEAT1 were co-located in the cytoplasm of HaCaT cells. The double-luciferase reporter gene assay showed that the relative activity of luciferase was significantly lower in the miR-485-5p group than in the negative control group (both P < 0.05) after the transfection with wild-type lncRNA NEAT1 or STAT3 recombinant plasmids, while there were no significant differences between the miR-485-5p group and negative control group after the transfection with mutant lncRNA NEAT1 or STAT3 recombinant plasmids (both P > 0.05). Compared with the control group, the lncRNA-NEAT1 overexpression group showed significantly increased expression of lncRNA NEAT1 and STAT3 (including STAT3 mRNA, STAT3 protein, and p-STAT3 protein) in HaCaT cells (all P < 0.05), but significantly decreased miR-485-5p expression ( P < 0.05) ; the Xidi Liangxue recipe group showed significantly decreased expression of lncRNA NEAT1 and STAT3 (all P < 0.05), but significantly increased miR-485-5p expression compared with the control group ( P < 0.05) ; significantly decreased expression of lncRNA NEAT1 and STAT3, but significantly increased miR-485-5p expression was observed in the Xidi Liangxue recipe + lncRNA-NEAT1 overexpression group compared with the lncRNA-NEAT1 overexpression group (all P < 0.05). After 24-, 48-, and 72-hour intervention, CCK8 assay showed that the proliferative activity of HaCaT cells was significantly higher in the lncRNA-NEAT1 overexpression group than in the control group (all P < 0.05), as well as in the Xidi Liangxue recipe + lncRNA-NEAT1 overexpression group than in the Xidi Liangxue recipe group (all P < 0.05), and the cellular proliferative activity was significantly lower in the Xidi Liangxue recipe + lncRNA-NEAT1 overexpression group and Xidi Liangxue recipe group than in the control group (all P < 0.05). The apoptosis rate was significantly lower in the lncRNA-NEAT1 overexpression group (5.84% ± 0.28%) than in the control group (14.75% ± 0.83%, LSD- t = 3.48, P = 0.002), but significantly higher in the Xidi Liangxue recipe group (35.72% ± 3.62%) than in the control group (LSD- t = 5.34, P = 0.001) ; the Xidi Liangxue recipe + lncRNA-NEAT1 overexpression group showed significantly increased apoptosis rate (27.64% ± 2.82%) compared with the lncRNA-NEAT1 overexpression group (LSD- t = 9.06, P < 0.001) . Conclusion:The Xidi Liangxue recipe could inhibit the proliferation of IL-17-induced HaCaT cells and promote their apoptosis, which may be related to the intervention in the lncRNA NEAT1/miR-485-5p/STAT3 regulatory network.

Objective:To investigate the effect of salvianolic acid on depressive behavior in depression model rats induced by chronic mild stress (CMS) and its mechanism.Methods:Fifty healthy male clean grade Sprague-Dawley(SD) rats were divided into five groups according to a random number table with 10 in each group: control group (nCMS+ Nal group), CMS+ normal saline group (CMS+ Nal group), CMS+ fluoxetine group (CMS+ Flu group), CMS+ salvia acid group (CMS+ Sal group), CMS+ fluoxetine+ Salvia acid group (CMS+ Flu+ Sal group). Except the control group, the rats in the other four groups were all received CMS modeling for 21 days. Twenty-one days after CMS modeling, rats were intraperitoneally injected with 0.9% normal saline (10 mg·kg -1·d -1), fluoxetine (20 mg·kg -1·d -1), salvia acid(40 mg·kg -1·d -1), fluoxetine(20 mg·kg -1·d -1)+ salvia acid(40 mg·kg -1·d -1)for 21 days. During the administration period, rats in the other four groups continued to receive CMS intervention for 21 days. Forced swimming test and sucrose preference test were conducted at baseline (day 0), after modeling (day 21) and after intervention (day 42) so as to evaluate depression like behavior. Then the rats were sacrificed and the hippocampus and prefrontal cortex were taken. The mRNA levels of Toll like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) were detected by RT-qPCR. The cytokines including interleukin-1β(IL-1β), interleukin-2(IL-2), interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) were detected by Luminex technique.SPSS 21.0 was used for statistical analysis.Repeated measurement ANOVA was used for behavioral data analysis, one-way ANOVA was used for molecular index data analysis, and Spearman was used for correlation analysis. Results:The results of repeated measurement ANOVA showed that the interaction effects between group and time of body mass, sucrose preference, forced swimming immobility time were significant at baseline, after modeling and after intervention ( F=18.238, 6.921, 7.591, all P<0.05). After modeling, compared with nCMS+ Nal group, the rats in CMS+ Flu group, CMS+ Sal group, CMS+ Flu+ Sal group and CMS+ Nal group had lower body weight, lower sucrose preference rate and longer forced swimming immobility time (all P<0.05). After intervention, compared with CMS+ Nal group(body weight (350.15±41.65)g, sucrose preference(52.95±11.13)%, static time(91.40±15.22)s), the body weight((378.21±30.78)g, (385.12±43.19)g, (391.41±31.21)g, (402.33±18.67)g, all P<0.05) and sucrose preference((69.30±15.56)%, (68.12±10.99)%, (71.18±9.51)%, (75.47±11.55)%, all P<0.05) of CMS+ Flu group, CMS+ Sal group, CMS+ Flu+ Sal group and nCMS+ Nal group were all increased, while the forced swimming immobility time ((68.81±21.74)s, (66.10±25.51)s, (63.53±22.32)s, (71.21±21.41)s, all P<0.05) were shorter (all P<0.05). After intervention, among the body weight, sucrose preference and the immobility time of CMS+ Flu group、CMS+ Sal group and CMS+ Flu+ Sal group, there were no differences between each two groups(all P>0.05). After intervention, the levels of TLR4 mRNA and MyD88 mRNA in prefrontal cortex and hippocampus of CMS+ Flu group, CMS+ Sal group, CMS+ Flu+ Sal group and nCMS+ Nal group were all lower than those in CMS+ Nal group (all P<0.05). In prefrontal cortex, the levels of TLR4 mRNA (0.715±0.358) and MyD88 mRNA (0.739±0.233) in CMS+ Flu+ Sal group were lower than those in CMS+ Sal group (1.943±0.606, 1.815±0.897) (both P<0.05). The level of TLR4 mRNA in prefrontal cortex and hippocampus of rats were positively correlated with the level of MyD88 mRNA and TNF-α level and forced swimming immobility time and negatively correlated with sucrose preference rate (prefrontal cortex r=0.915, 0.041, 0.027, -0.178, all P<0.05; hippocampus r=0.810, 0.070, 0.011, -0.153, all P<0.05). Conclusion:The antidepressant effect of salvianolic acid is presumedly achieved by inhibiting the immunoinflammatory response mediated by the TLR4/Myd88 signaling pathway in CMS rats.

Objective To investigate the effect of prenatal stress (PS) at different pregnant time on emotion and cognition of adult offspring rats.Methods Twelve healthy female Sprague Dawley (SD) rats were randomly divided into control group(CON,n=4),the early pregnancy group(PS1,the 1～ 7 days of pregnancy,n=4) and the late pregnancy group(PS3,the 15 ～ 21 days of pregnancy,n=4).The pregnant rats were exposed to single-prolonged stress(SPS) on gestational day 7 or 15 respectively,except control group.The offspring were measured every weekend from 1-7 week after birth.At the eighth weekend,the sucrose intake (anhedonia) and Morris water maze (MWM) were performed to assess depression-like behavior and spatial learning and memory.Results The body weight of the first to seventh weeks after birth showed that there was a statistically significant difference among the three groups (F=28.207,P＜0.01),and there was a significant difference in time effect (F=1 041.546,P＜0.01).The body weight of two PS groups was significantly lower than those of control group(P＜0.05).The body weight of PS3 was lower than that of PS1 significantly(P＜0.05).Sucrose preference:PS3((27.70± 19.31) ％) were reductive on sucrose consumption than CON significantly((66.93±19.67) ％)(P＜0.05)while PS1 ((89.80±6.79) ％) increased in sucrose consumption compared with the CON significantly(P＜0.05).MWM:in training stage the difference of average avoid latency was existed in the three groups of the first 5 days(F=11.121,P＜0.01).Similarly,there was a significant difference in measure time(F=91.327,P＜0.01),the escape latency of the PS3 was decreased,while PS1 was significantly increased compared with CON;in testing stage,PS3 ((54.50±4.64) s,(53.21±4.45)) showed a significant increase in the duration in target site and numbers of times across the target site compared with CON((32.24±.4.17) s,(31.68±4.00)) (P＜0.05).Conclusion The acceptance of stress in the late pregnancy may lead to depression like behavior in the adult offspring and also enhance the learning and memory ability.And acceptance of stress in early pregnancy can cause impairment of learning and memory ability in adult offspring rats.

Objective To explore the correlation between childhood trauma and plasma adiponectin levels in patients with depression.Methods A total of 121 patients with depression and 39 healthy controls(control group)were enrolled.Childhood trauma questionnaire(CTQ-SF)was used to assess the experience of childhood abuse and neglect,and the patients with depression were divided into trauma group(n=53)and non-trauma group(n=68)according to the CTQ-SF score.The 17-item Hamilton depression scale-17(HAMD17)and the Hamilton anxiety scale(HAMA)were used to evaluate the severity of depression and anxiety symptoms,respectively.Plasma adiponectin levels of subjects were measured by enzyme-linked immunosorbent assay.Results The plasma adiponectin level of trauma group[3.82(2.44,4.92)μg/mL]was significantly lower than that of non-trauma group[4.64(2.98,6.43)μg/mL,P=0.01]and the control group[6.29(4.54,7.51)μg/mL,P＜0.01].The plasma adiponectin level of non-trauma group was lower than that of the control group(P＜0.01).Correlation analysis showed that plasma adiponectin level in patients with depression was negatively correlated with childhood trauma(r=-0.34,P＜0.01).Multivariate linear regression analysis showed that plasma adiponectin level was negatively correlated with childhood trauma scores in patients with depression(β=-0.05,P＜0.01).Conclusions Patients with depression who have experienced childhood trauma have lower plasma levels of adiponectin,and childhood trauma may be associated with decreased plasma adiponectin levels in patients with depression.