Objective To investigate the change of transforming growth factor-?1 (TGF-?1) in peripheral blood in patients with bronchial asthma and the effect of traditional Chinese medicine Ligustrazine on it. Methods We recruited 80 normal healthy people as the control group and 160 hospitalized patients, including 80 moderate cases and 80 severe cases of bronchial asthma. TGF-?1 in peripheral blood of the patients was detected by enzyme linked immunosorbent assay. The patients were treated with conventional therapy or conventional therapy added Ligustrazine; TGF-?1 in peripheral blood before and after treatment was detected and compared. Results The level of peripheral blood TGF-?1 was higher in the patient group than in the control group obviously (P

Objective To study the effect ofoxymatrine on serum matrix metalloproteinase-9 (MMP-9)and transforming growth factor-β 1 (TGF-β 1) in patients with idiopathic pulmonary fibrosis (IPF) and illuminate the mechanism and action.Methods Total 38 patients with IPF in the patient group were divided into the conventional treatment group and the oxymatrine group by random digits table method with 19 cases each.Meanwhile 38 healthy people were as the control group.Then serum MMP-9 and TGF-β1 levels were detected by enzyme-linked immunosorbent assay and compared.Results The serum MMP-9 level in the control group and the patient group was (92.30 ± 27.21),(420.66 ± 101.78) μg/L,and there was significant difference (P ＜ 0.05).The serum TGF-β 1 level in the control group and the patient group was (67.36 ± 13.03),(217.82 ±43.90) μg/L,there was significant difference (P ＜0.05).There was no significant difference in the serum MMP-9 and TGF-β1 level before treatment between the conventional treatment group and the oxymatrine group (P ＞ 0.05).There was significant difference in the serum MMP-9 level before and after treatment in the conventional treatment group [(138.91 ± 35.09) μ g/L vs.(428.21 ±102.75) μ g/L] (P ＜ 0.05).There was no significant difference in the serum MMP-9 level before and after treatment in the oxymatrine group (P ＞ 0.05).There was significant difference in the serum TGF-β 1 level before and after treatment in the conventional treatment group and the oxymatrine group [(145.42 ± 30.78)μg/Lvs.(200.34±58.96)μg/L;(102.37±26.04) μg/Lvs.(219.78±63.20) μg/L](P＜0.05).There was significant difference in the serum TGF-β1 level after treatment between the conventional treatment group and the oxymatrine group (P＜ 0.05).Conclusion Oxymatrine can degrade IPF by reducing TGF-β 1 and maintaining MMP-9 in the higher level.

Objective To explore the expressions of cardiac protein kinase C(PKC),IGF-1(insulin-like growth factor 1) and the effect of drugs in the process of left ventricular remodeling(LVRM).Methods SD rats were randomly divided into four groups: sham operation group,infracted group,Captopril group and Valsartan group.Except for sham operation group,left anterior descending coronary artery was ligated in all rats of the other three groups and the intragastric administration of solvent,100 mg?kg~(-1)?d~(-1) Captopril and 20 mg?kg~(-1)?d~(-1) Valsartan was done on day 3 after operation for 8 weeks,then LVRM was evaluated by pathologic analysis.Expression changes of cardiac AgT_(1)R,PKC,and IGF-1 were detected by immunohistochemistry and computer image analysis.IGF-1 mRNA expression was analyzed by RT-PCR.Results LVW,LVWI and the expressions of AgT_(1)R,PKC,IGF-1 mRNA and proteins were significantly enhanced(P

Aim To research the effects of HSP70 in-hibitor ( PFTμ) on the expressions of iNOS induced by IFN-γ in RAW 264. 7 cells. Methods The NO con-centration was measured by Griess Kit. The expression of interest protein was measured by Western blot and iNOS mRNA was measured by RT-PCR. Mouse cardi-ac ischemia-reperfusion ( I/R ) model was established to set up the inflammatory response. These were divid-ed into control and treated groups. The infarct size was monitored on myocardial I/R mice. Results We found that PFTμsignificantly blocked the production of NO and the expression of iNOS protein and mRNA in RAW 264. 7 cells. The mechanism may be part of the inhibition of nuclear IRF-1 protein expression. We also found that PFTμ reduced the infarct size in myocardial I/R mice ( P <0. 05 ) . Conclusion These results suggest that PFTμ down-regulates the IFN-γ-induced iNOS transcription through decreasing translocated IRF-1 protein.

Objective To study the cause,clinical characteristics and treatment of HFmrEF,HFrEF and HFpEF patients.Methods Three hundred and eighty-five heart failure (HF) patients aged ≥60 years admitted to our hospital from January 2016 to March 2017 were divided into HFrEF group (n=96),HFmrEF group (n=34) and HFpEF group (n=255) according to their ejection fraction.Their demographic data,HF cause,clinical characteristics,cardiac ultrasonographic data,laboratory testing data and therapies were recorded.Their clinical characteristics were compared.Results The number of males was greater and the cardiac function grade Ⅳ was higher in HFmrEF group than in HFrEF and HFpEF groups.The incidence of hypertension was the highest followed by that of valvular disease.The number of HFmrEF patients who used intravenous nitrates,spironolactone and milrinone was greater than that of HFpEF and HFrEF patients who used intravenous nitrates,spironolactone and milrinone.The serum creatinine level was higher in HFmrEF patients than in HFpEF and HFrEF patients at the time when they were discharged.Conclusion Hypertension and valvular disease are the mian risk factors for HFmrEF.The number of males is greater and the cardiac function grade Ⅳ is higher in HFmrEF patients than in HFrEF and HFpEF patients.The serum creatinine level is higher and the outcome is better in HFmrEF patients than in HFrEF and HFpEF patients at the time when they are discharged.

In the present study, the specifically knockdown models of P-gp or MRP2 were constructed by using a series of chemically synthesized small interfering RNA (siRNA) in vitro. The expression of P-gp and MRP2 was measured by real-time PCR and Western blot, and the function was evaluated by applying P-gp and MRP2 substrate, rhodamine and methotrexate. The results showed that MRP2 siRNA-3 or P-gp siRNA-2 significantly decreased the mRNA expression of MRP2 or P-gp, the inhibition ratio was 68% or 84%; MRP2 siRNA-3 or P-gp siRNA-2 at a dose of 80 nmol x L(-1) significantly reduced the protein expression of MRP2 or P-gp at 48 h after treatment, the inhibition ratio was 62% or 70%. Meanwhile, other transporters were not influenced by siRNA. When pretreatment with MRP2 siRNA-3 or P-gp siRNA-2, the efflux of methotrexate or rhodamine decreased significantly and the intra-cellular concentration increased. The results suggested that chemically synthesized siRNA could significantly inhibit the expression and function of MRP2 and P-gp, and the model of RNAi in vitro could be used to evaluate the role of efflux transporters in transportation of drugs.

Objective To determine the effects of intrauterine growth retardation(IUGR) caused by malnutrition during pregnancy on the lung structure and expression of Clara cell protein (CCSP) and interferon (IFN)-γ in the fetal lungs,and to explore their relation ship with pulmonary disease.Methods Fetal rats from maternal protein-malnutrition dams were studied on day 20(term 21.5 day).The lung pathology was examined by means of Hematoxylin and eosin(HE) stain.Plasma was collected to determine the CCSP and IFN-γ concentration.Lungs were harvested to measure the expression of CCSP and IFN-γ mRNA by using fluorescent quantization reverse transcription (RT)-PCR and the levels of CCSP and IFN-γ protein were assessed by using enzyme-linked immunosorbent assay.Results Malnutrition fetus body weight significantly less compared to control group,so did the lung weight.However,lung weight,expressed as a percentage of body weight between the 2 groups was not different.The IUGR group had significantly decreased alveolar number manifested by lower radial alveolar count,and significantly increased mean linear intercept of alveoli.Both the CCSP mRNA expression and protein level in lung of IUGR rats were decreased compared with control rats (all P ＜ 0.05).A decline in plasma CCSP protein concentration was also noted compared with control group (P ＜0.05).Furthermore,IUGR group fetus showed lower IFN-γ levels both in circulation and in the lung tissue (all P ＜ 0.05).Conclusions Intrauterine malnutrition significantly alters lung structure and cytokine IFN-γ level,and the latter may further inhibit the transcription of CCSP gene.These alterations may contribute to both early and late postnatal respiratory morbidity.

Objective To compare the surgical outcomes between laparoscopic and open surgeries in treatment of ectopic oviduct pregnancy, and investigate the clinical value of laparoscopic surgery. Methods Two hundred and forty-six patients with ectopic oviduct pregnancy in our hospital from June 2009 to March 2013 were retrospectively analyzed. 134 cases were treated with laparoscopic operation and 112 with open surgery. Some parameters such as operative time, blood loss, usage of pain-killer, hospital stay were compared between both groups. Results All operations were successful. Laparoscopic surgery was shown to be superior to open operation in the parameters of operative time, blood loss, usage of pain-killer and hospital stay ( < 0.05) . Conclusion Compared with open operation, laparoscopic surgery has the advantages of less trauma and rapid postoperative rehabilitation. It may become the first line treatment for ectopic oviduct pregnancy.

Object To study the origin, morphology and histology of Galla Cinnamomi Camphorae(GCC). Methods By the literature investigation and the survey in the production area, GCC was identified by microscopic technique. Results The origin and the medicinal part of GCC were defined. Conclusion GCC is the abnormal fruit of Cinnamomum camphora (L.) Presl which has been infected by Exobasidium sawadae Yamada and formed with hymenium and fruit. The characters in morphology and histology of GCC provide the scientific reference of identification of the crude drug.

Objective To investigate the role of NF-κB activation in the inflammatory mechanism of chronic obstructive pulmonary disease (COPD).Methods Monocyte were collected from patients with COPD and were cultured,and stimulated with lipopolysaccharide (LPS) ; NF-κB p65 activation was measured by immunohistochemistry; SOD ,MDA and IL-8 and lung function were determined synchronously.Results The NF-κB p65 was induced by LPS in monocyte in all subjects, but it was most markedly done in COPD patients with exacerbateions; There was positive correlation between the NF-κB p65 activation of monocytes and levels of IL-8 and MDA in circulation, but it was negative correlation to SOD.Conclusion NF-κB plays a vital role in regulating product of IL-8 in monocyte in COPD.