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Objective To explore the clinical curative effect of theTaohong-Siwu decoction combined with manipulation in the treatment of the acute phase of lumbar disc herniation (LDH) and its effect on serum inflammatory factors.Methods According to the random number table method, 102 patients with the acute phase of LDH were divided into control group and research group from May 2014 to September 2016, 51 cases in each group. Patients in control group were treated by traction and non-steroidal anti-inflammatory drug for a month, while patients in research group were treated by manipulation combined withTaohong-Siwu decoction for a month. After treatment, the overall efficacy was observed. The Visual analogous scale (VAS) and JOA scores were recorded before and after the treatment. The IL-1β, IL-6 and TNF-α levels of inflammatory factors were detected by enzyme-linked immunosorbent assay.Results The total effective rate of patients in research roup was significantly higher than that of the control group [90.20％ (46/51)vs. 43.14％ (22/51),χ2=19.329, P=0.006]. After treatment, the VAS scores of patients in both groups were significantly decreased, and JOA score increased markedly, which the differences were statistically significant (Ps<0.05). After treatment, the VAS score of research group was significantly lower than the control group (4.26 ± 0.56vs. 5.13 ± 0.87;t=4.843, P=0.027), and JOA score was significantly higher than the control group (18.42 ± 3.92vs.17.33 ± 4.21;t=5.127, P=0.022). After treatment, the IL-1β, IL-6 and TNF-α levels of of patients in the research group were significantly lower than those of the control group (0.57 ± 0.11μg/Lvs. 0.90 ± 0.13μg/L, 112.26 ± 15.17μg/Lvs. 130.38 ± 18.29μg/L, 2.01 ± 0.34μg/Lvs. 2.37 ± 0.51μg/L;t=5.429, 6.317, 5.011,P<0.05). ConclusionsThe Taohong-Siwu decoction combined with manipulation on treatment of the acute phase of LDH was effective. The combined therapy can improve the VAS score and JOA score, and reduce the levels of inflammatory cytokines.
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<p><b>BACKGROUND</b>Phosphatase and tensin homologue on chromosome ten (PTEN) acts as a convergent nodal signalling point for cardiomyocyte hypertrophy, growth and survival. However, the role of PTEN in cardiac conditions such as right ventricular hypertrophy caused by chronic hypoxic pulmonary, hypertension remains unclear. This study preliminarily discussed the role of PTEN in the cardiac response to increased pulmonary vascular resistance using the hypoxia-induced PH rats.</p><p><b>METHODS</b>Male Sprague Dawley rats were exposed to 10% oxygen for 1, 3, 7, 14 or 21 days to induce hypertension and right ventricular hypertrophy. Right ventricular systolic pressure was measured via catheterization. Hypertrophy index was calculated as the ratio of right ventricular mass to left ventricle plus septum mass. Tissue morphology and fibrosis were measured using hematoxylin, eosin and picrosirius red staining. The expression and phosphorylation levels of PTEN in ventricles were determined by real time PCR and Western blotting.</p><p><b>RESULTS</b>Hypoxic exposure of rats resulted in pathological hypertrophy, interstitial fibrosis and remodelling of the right ventricle. The phosphorylation of PTEN increased significantly in the hypertrophic right ventricle compared to the normoxic control group. There were no changes in protein expression in either ventricle.</p><p><b>CONCLUSION</b>Hypoxia induced pulmonary hypertension developed pathological right ventricular hypertrophy and remodelling probably related to an increased phosphorylation of PTEN.</p>
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Animals , Male , Rats , Hypertension, Pulmonary , Metabolism , Hypertrophy, Right Ventricular , Metabolism , Hypoxia , Metabolism , PTEN Phosphohydrolase , Metabolism , Phosphorylation , Rats, Sprague-DawleyABSTRACT
Objective To evaluate the effect of the activity of Ca2+/CaN-NFATc on the activation and prolfferation of lymphocyte in asthmatic rats.Methods The rats of the asthma group and the CsA group were sensitized and challenged by ovalbumin.So did the control group with saline instead.Lymphocyte was separated from spleen and cultured for 24 hours,and PHA-p (5 μg/ml) was added to the culture medium in every group,CsA ( 1.0 μg/ml) was added to the CsA group,respectively.The concentration of [ Ca2+ ] i,the activity of CaN,the protein expression of dephosphorylated NFATc and Cyclin E in T lymphocyte were assayed.The level of IL-4 and IL-2 in culture supernatants was measured,and the cell cycle distribution of lymphocyte was analyzed.ResultsWhen compared to the control group,the activity of Ca2+/CaN-NFATc [ (81.21 4-14.39) vs (63.66 ±9.02) ] was increased and the protein expression of CyclinE [ (0.9327 ±0.0370) vs (0.8374 ±0.0637) ] was higher in Lymphocyte of the asthma group ( P＜0.05,P ＜0.01,respectively).The percentage of lymphocyte in the S phase [ (7.8600±2.8241) vs (4.0270 ± 1.8650) ] and S + G2/M phase [ ( 10.6700±3.3850) vs (5.8740 ± 1.4389) ] was higher;however,the percentage of G0/G1 phase [ (89.3300 ± 3.3850) vs (94.1260± 1.4389 )] was lower in asthma group ( all P ＜ 0.01 ).The level of IL-4 [ ( 1.55 ± 0.19) pg/ml vs (0.99 ± 0.12 ) pg/ml ] and the IL-4/ IL-2 ratio [ (0.81 ±0.12) vs (0.49 ±0.49) ] in culture supernatants of the asthma group were higher than those of the control group ( all P ＜0.01 ).While the activity of Ca2+/CaN-NFATc (47.19 ±7.16)was decreased and the protein expression of Cyclin E (0.6840 ± 0.0485 ) was reduced in lymphocyte in CsA group(all P ＜0.01 ),the percentage of lymphocyte in the S phase (4.8600 ± 1.9595) and S + G2/M phase (7.9900 ± 1.9405) was decreased and the percentage of G0/G1 phase (92.2100 ± 1.9267) was increased ( all P ＜ 0.05 ),and the level of IL-4 (0.47 ± 0.09 ) pg/ml and the ratio of IL-4/ IL-2 (0.78 ±0.20) was lower in culture supernatants in the CsA group than that of the asthma group( all P ＜ 0.01 ).There was a positive correlation between the protein expression of dephosphorylated NFATc and the protein expression of CyclinE in Lymphocyte,so did between the protein expression of NFATc and the level of IL-4 in culture supernatants( r =0.711,P ＜0.01 and r =0.749,P ＜0.01.respectively).Conclusions The activity of Ca2+/CaN-NFATc was increased in lymphocyte of the asthmatic rats.Its increasing might result in the imbalance of Th1/Th2 by promoting the expression of IL-4 and might lead to the proliferation of lymphocyte by promoting the Cyclin E expression.
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ObjectiveTo investigate the effects of nicotine on the expression of Th1/Th2 cytokines and transcription factor T-bet/GATA-3 in cultured CD4+ T of rat sensitized by ovalbumin.Methods Two weeks after immunization by ovalbumin,splenic CD4+ T cells of Wistar rat were purified using CD4+T cell enrichment kit.Purified CD4+ T cells of rat were cultured and divided into 4 groups:a control group,1 μg/ml nicotine stimulated group,10 μg/ml nicotine stimulated group,100 μg/ml nicotine stimulated group.These cells,in their groups,were stimulated with or without nicotine and were all challenged simultaneously with OVA.Supernatants and cell pellets were harvested after being stimulated for 24 h.The concentration of IFN-γ and IL-4 in supernatants were measured by enzyme-linked immunosorbent assay (ELISA).Real-time PCR was used to determine the mRNA expression of T-bet and GATA-3 in CD4+T cells.Results ( 1 ) IFN-γproduction was significantly decreased in all nicotine treated groups [ ( 113.78±6.06) ng/L,(70.31±7.26) ng/L,(20.00±2.14) ng/L] compared with the control group[ (142.30± 5.89) ng/L],and the level of IL-4 was significantly increased in all nicotine treated groups [ (69.49±3.91) ng/L,(93.63±4.56) ng/L,(50.97±3.07) ng/L] compared with the control group[ (36.91±3.24) ng/L].(2) Expression of T-bet mRNA in all nicotine treated groups(0.73±0.03,0.57±0.04,0.31 ±0.00) was lower than that in the control group(0.98±0.09),but expression of GATA-3 mRNA in all nicotine treated groups (4.31±0.26,5.16±0.23,1.56±0.14) was significantly higher than that in the control group(1.00±0.07).Conclusion Nicotine may play a key role in the development of Th2-type allergic inflammation in asthma by promoting over-expression of GATA-3 mRNA and downregulating the expression of T-bet mRNA.
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Objective To investigate the change characteristics of the brain neurotransmitters of human with stress events by the Encephaloflucgram technology (ET) at the noninvasive condition. Methods Extract shocking informations with neurotransmitter requlation systems in EEG ( S spectral line) by ET and analyze thechange characteristics of the brain neurotransmitters of human with stress events, the clincial symptons of the patients were evaluated by the post-traumatic stress disorder-check scale (PCL-C). Results ①Compared with expected number,the activity of neurotransmitters such as γ-aminobutyric acid (GABA) were significantly decreased (4.64 ±2.88,8.45 ±0.42, P＜0. 01 ) and the activity of neurotransmitters such as dopamine( DA ) ( 17.01 ±7.41,7.59±0.55, P＜0. 01),acetylcholine(Ach) (17.01 ±7.41,14.95 ±0.65, P＜0.05) ,norepinephrine (NE ) ( 13.07 ± 4.33,11.82 ± 0.84, P ＜ 0. 05 ) were increased. ②There was a significant difference on GABA ( t =6.902, P ＜ 0. 01 ) between suspect of post-traumatic stress disorder and non-post-traumatic stress disorder. ③In PCL-C scale score, intrusion factor had negative correlation to the activity of GABA ( r = - 0.777, P ＜ 0.01 ), and positive correlation to the activity of DA ( r = 0.360, P ＜ 0.01 ), hyper-arousal factor was positive correlated with the activity of NE ( r=0.221, P＜0.05) ,escaping/numbness factor was negative correlated with the activity ofGlu( r= -0.274, P＜0.05). Conclusion In traumatic stress events GABA,Ach,DA,NE neurotransmitters aresignificantly changed ,and meybe participat stress responses.
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Objective To investigate the impact of cigarette smoking on inflammatary factors in sputum including cell component,IL-8 and eotaxin,and the effect on responses to treatment with inhaled corticosteroids (ICS)in patients with asthma.Methods Thirty-eight outpatients with chronic stable asthma who visited from January 2009 to February 2010 were enrolled in the study.Twenty-three cases were nonsmokers and 15 cases were smokers.All of them were treated by daily inhaled budesonide,and[32 agonist when necessary.Induced sputum eosinophil and neutrophil proportion were measured,and the levels of interleukin(IL-8)and eotaxin in induced-sputum by enzymatic immunoassay(ELISA)were compared between non-smoking and smoking asthmatic patients.Results The eosinophil proportion was(2.0 ± 0.4)％ in smokers and(4.6 ± 2.5)％ in nonsmokers before therapy,and(1.1 ± 0.5)％ in smokers and(1.8 ± 0.6)％ in nonsmokers after therapy.The difference was statistical significant(F =15.271,P ＜ 0.05).The eotaxin was(3.5 ± 2.1)× 10-3 mg/L insmokers and(8.6 + 2.3)x 10-3 mg/L in nonsmokers before therapy,and(3.1 + 1.5)x 10-3 mg/L insmokers)and(3.6 ± 1.3)x 10-3 mg/L in nonsmokers after therapy.There was statistical significant(F =24.172,P ＜ 0.05).There were no significant difference on neutrophil proportion and IL-8 before and after treatment(F =1.563 and 1.793,respectively,Ps ＞ 0.05).Neutrophil proportion(F =9.632,P ＜ 0.05)and IL-8(F =5.720,P ＜ 0.05)in smokers were significantly higher than non-smokers,whereas eosinophil proportion (F =15.879,P ＜ 0.05)and eotaxin(F =12.365,P ＜ 0.05)in smokers were significantly lower than nonsmokers.Conclusion There was a significantly increase in inflammatary cells andfactors in induced-sputum in two groups after ICS treatment,but the effect in smokers was lower than in non-smokers.Neutrophil proportion and IL-8 were higher in induced sputum in smokers,whereas eosinophil proportion and eotaxin were higher in non-smokers.
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ObjectiveTo explore the influence of the cigarette smoke in the airway inflammation and pulmonary function of the asthmatic patients. MethodsTwenty-five cases of asthmatic patients with cigarette smoke exposure, 22 cases of asthmatic patients without cigarette smoke exposure and 20 cases of normal control persons were involved in this study. The proportion of various inflammatory cells in the induced sputum, the levels of serum interleukin (IL)-8 and IL-4 and lung function (FEV1％ expected value,FEV1/ＦVC％ ) were detected. ResultsThe infiltrating of neutrophils was primarily found in sputum of the asthmatic patients with cigarette smoke exposure, but the infiltrating of eosinophils was mainly in sputum of the asthmatic patients without cigarette smoke exposure. The levels of serum IL-8 and IL-4 of peripheral blood of asthmatic patients with cigarette smoke exposure[(277.02 ±71.37), (171.69 ±31.01) ng/L] were significantly higher than those in asthmatic patients without cigarette smoke exposure[(158.88 ± 21.95 ),( 111.42 ± 21.69 ) ng/L] and normal control persons [( 116.78 ± 71.37 ), (73.94 ± 15.72 ) ng/L] (P ＜ 0.01 ).The FEV1％ expected value and FEV1/FVC％ of the asthmatic patients with cigarette smoke exposure [(51.12 ± 13.30) ％, ( 49.16 ± 11.09 )％] was lower than those of asthmatic patients without cigarette smokeexposure [(81.81 ± 5.82)％, (79.00 ± 3.86)％] and normal control persona [(95.50 ± 10.11 )％, (83.18 ±6.04)％] (P ＜ 0.01 ). The level of serum IL-8 was positively correlated to the neutrophils percentage in the induced sputum (r =0.742,P＜ 0.01 ) ,while negatively correlated to the FEV1％ expected value(r =-0.739,P ＜ 0.01 ). ConclusionCigarette smoke may influence the airway inflammation of the asthmatic patients and accelerate the deterioration of their lung function by promoting the producing of IL-8.
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Objective To evaluate the activity of Ca2+ /CaN-NFATc, and study its association with the imbalance of TH1/ TH2 in asthmatic rat lungs. Methods Twenty-four Wistar rats were random divided to the asthma group and control group, twelve rats each group. The rats were sensitized and challenged with ovalbumin to establish the asthmatic model. The pulmonary function of rats was surveyed and evaluated u-sing Maclab system. Airway inflammation and the thickness of bronchial wall ( WAt/Pi) were observed by H. E staining. The quantity of Ca2+ , the activity of CaN , the protein expression of dephosphorylated NFATc and the level of IL-4 and IL-2 were assayed.Results Compared with control group, the thickness of bronchial wall was significantly increased ( t = -7. 99, P <0. 01), the airway resistance was higher( t = 2.59, P <0.05) and the respiration frequency was faster( t =7.94, P <0.01) ,but the minute ventilation volume was lower( t =6. 87, P <0.01) in asthma group. The levels of IL-4 and the IL-4/ IL-2 ratio in rat lungs of asthma group were significantly higher than those in control group ( t = -8.69, P <0. 01; t = 11.40, P <0. 01 .respectively) , however, the levels of IL-2 in asthma group were lower than that in control group ( t =8. 29, P <0. 01). The activity of CaN and the protein expression of dephosphorylated NFATc in asthma group were higher than those in control group( t = -2. 91, P <0.01; t = -22.45, P <0.01,respectively) ,but the quantity of Ca2+ in asthma group was lower than that in control group( t =4. 747, P < 0.01). There wag a positive correlation between the activity of CaN and the protein expression of dephos-phorylated NFATc( r =0. 39, P <0.05) ,so did between the protein expression of dephosphorylated NFATc and the IL-4/ IL-2 ratio( r =0. 83-, P <0.01) ,and the same between the thickness of bronchial wall and the IL-4/ IL-2 ratio( r = 0. 84, P < 0.01). Conclusions The activity of CaN-NFATc was increased in rat lungs of asthma group, and the rising of which might increase the ratio IL-4/ IL-2. Thus, the signal of CaN-NFATc probably took part in the imbalance of TH1/ TH2 in asthmatic rat lungs.
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Objective To observe the content of macrophage inflammatory protein-1α(MIP-1α)in plasma and bronchoalveolar lavage fluid (BALF) and the expressions of MIP-1α mRNA and nuclear factor-kappa B( NFκB)p65 mRNA in the lung of rats subjected to mechanical ventilation with high tidal volume. Method Thirty-two healthy Wistar rats were randomly ( random number) divided into control group, ventilator induced lung injury (VILI) group,dexamethasone (DEX) group and budesonide (BUD) group. The content of MIP-1α in plasma and BALF were measured with ELJSA and the expressions of MIP-1α mRNA and NF-κBp65 mRNA in lung of rat were detected by RT-PCR. The data distributed were expressed as (-x) ± s and were compared among 4 groups. Furthermore, the correlation between the content of MIP-1α and the expression of MIP-1α mRNA, and the correlation between the expression of MIP-1α mRNA and the expression of NF-κBp65 mRNA were analyzed in the latter three groups. Results With lessened lung injury ,the content of MIP-1αin plasma and BALF and the expressions of MIP-1α mRNA and NF-κBp65 mRNA in lungs of rats of DEX and BUD groups were significantly lower than those in VILI group ( P ＜ 0.001 ). Although the content of MIP-1α in plasma and BALF and the expressions of MIP-1α mRNA and NF-κBp65 mRNA in lungs of rats of BUD group were higher than those of DEX group, but no significant differences were found between them ( P ＞ 0.05). Correlation study showed that positive correlations were xisted between the MIP-1α in plasma and the expression of MIP-1α mRNA in the lungs ( r = 0.895, P ＜ 0.05)and between the expression of MIP-1α mRNA and the expression of NF-κBp65 mRNA in the lungs ( r=0.801, P ＜ 0.05). Conclusions Glucocorticoid could down-regulate the expression of MIP-1α mRNA by inhibiting the activity of NF-κB in the lungs and may have preventive and therapeutic effect to VILI to some extent. The effect of glucocorticoid used locally against VILI is simnilar to that of systemic administration with lesser adverse reactions.
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Objective To investigate the effects of different tidal volume ventilation on acute lung injury in rats. Methods Thlrty-two normal Wistar rats were randomly divided into four groups:control group,low tidal volume group(L- V_T),conventional tidal volume group(C-V_T)and high tidal volume group(H-V_T).The pathologic changes of the lungs were observed under macrography,light and electron microscope.The blood gas analysis(PaO_2),the counts of neutrophils (PMN),the levels of protein and the myloperoxidase(MPO)activities in bronchoalveolar lavage fluid(BALF)were measured by biochemical methods respectively.Results There were no distinct pathological differences between L-V_T group and control group under macrography,light and electron microscope.In the C-V_T and H-V_T groups,there were different degree of lung injuries under light and electron microscope,their PMN,MPO activity and protein level in BALF were significantly higher than those of control and L-V_T groups and their PaO_2 were significantly lower than those of control and L- V_T groups(P＜0.01,P＜0.05).The MPO activity and the protein level in BALF were also significantly higher than those of C-VT group(P＜0.01)Of the above indexes,there were no statistical differences between L-V_T group and control group(P＞0.05).Conclusion Conventional tidal volume ventilation alone,without any lung-protective strategy, could produce injuries to the normal lung tissues,while low tidal volume ventilation hadn't effects on them.The injury effects produced by mechanical ventilation was closely related to the recruitment and activation of neutrephils in the lung.
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AIM: To investigate the expression of interleukin-13 (IL-13) in lung tissue of rat asthmatic model and effect of triptolide on expression of IL-13. METHODS: A asthmatic model was established and inflammation changes of lung tissues were examined by haematoxylin-eosin staining. Reverse transcriptio polymerase chain reaction (RT-PCR) was used to semiquantitate the expression of IL-13 mRNA, and enzyme-linked-immuno-sorbent assay (ELISA) was used to detect protein level of IL-13. RESULTS: There was a significant increase in the count of EOS, the expression of IL-13 mRNA and IL-13 protein level in lung tissue of asthmatic rats compared with those of triptolide-treated rats (P0.05). The expression of IL-13 mRNA and IL-13 protein level in triptolide-treated rats were significant lower than that of asthmatic rats (P
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AIM:To observe the expression of cyclin E in the lungs of asthmatic rats and to evaluate the role of cyclin E in airway remodeling with asthma. METHODS:Twenty Wistar rats were randomized to the asthma group and control group (10 rats in each group). The rats were sensitized and challenged with ovalbumin to establish the asthmatic model. Airway inflammation was observed by HE staining. The thickness of the bronchial wall (WA/Pi) was measured by computer-assisted image analysis system. The cell cycle distribution of monocytes in peripheral blood was analyzed by flow cytometry. The mRNA expression of cyclin E was detected by realtime RT-PCR. The protein expression of cyclin E was assayed by Western blotting and immunohistochemistry. RESULTS:The thickness of the bronchial wall in asthma group was significantly higher than that in control group (P