ABSTRACT
【Objective】 To explore the effect of B lymphocytes on cardiac structure and function and myocardial immune cells during heart development. 【Methods】 Echocardiography, immunofluorescence staining and flow cytometry were used to evaluate the composition of immune cells of the heart and the cardiac structure and function in wild-type (WT) mice and B-lymphocyte-deficient (μMT) mice, respectively. 【Results】 Compared with those of μMT mice, the ratio of heart weight to mouse weight (P<0.05), left ventricular mass (P<0.05) and the cross-sectional area of myocardial cells WT mice were significantly increased, while the ventricular ejection fraction was significantly decreased (P<0.05). The results of mRNA sequencing showed that WT mice and μMT mice differentially expressed genes were mainly enriched in the signal pathway of heart development and hypertrophic cardiomyopathy. The results of flow cytometry showed that WT mice had more Ly6g+ neutrophils, CD4+ positive T cells (P<0.001) and CD8+T cells (P<0.05) compared with μMT mice. 【Conclusion】 B-lymphocyte depletion alters the composition of cardiomyocyte immune cells, reduces left ventricular mass, and increases myocardial contractility.
ABSTRACT
【Objective】 To explore B lymphocytes’ role and mechanisms in angiotensinⅡ/phenylephrine (AngⅡ/PE) induced cardiomyopathy so as to understand the role of inflammatory cells in myocardial injury. 【Methods】 AngⅡ/PE was administered to wild-type (WT) and B cells deficiency (μMT) mice for 14 days or 28 days. The mice were analyzed by blood pressure measurement, echocardiography imaging, flow cytometry, and histology. Cardiac fibrosis was evaluated by Masson staining. 【Results】 Compared with the control group, the left ventricular mass (P<0.01), heart mass/tibia length ratio (P<0.01) and cross-sectional area of cardiomyocytes in AngⅡ/PE group were significantly increased (P<0.01). After 2 weeks of AngⅡ/PE treatment, B lymphocytes (P<0.05), CD45+ leukocytes (P<0.05), CD64-Ly6C+ monocytes (P<0.05), CD64+Ly6C-macrophages (P<0.05) and Ly6g+ neutrophils (P<0.05) were recruited in myocardial tissue. Compared with WT_AngⅡ/PE group, the heart weight/tibia length ratio (P<0.05), left ventricular weight (P<0.05) and myocardial cell cross-sectional area (P<0.05) of μMT_AngⅡ/PE mice were significantly improved. CD45+Ly6C+CD64- monocytes (P<0.05) and CD45+Ly6C-CD64+ macrophages (P<0.05) were significantly decreased. 【Conclusion】 B lymphocytes deficiency improves AngⅡ/PE induced cardiac hypertrophy by reducing the infiltration of CD45+Ly6C+CD64- monocytes and CD45+Ly6C- CD64+ macrophages.
ABSTRACT
To observe the immunogenicity of hPDGF-B immunogens that were synthesized with the fusional expression vector pET28-Trx and to test the suppressive effect of these specific antibodies induced by both of immunogens on proliferation of human HepG2 hepatoma cells. First, we chose 2 antigenic epitopes hPDGF-BΔ103-118aa and hPDGF-BΔ152-167aa from human PDGF-B and inserted these 2 coding regions into the empty vector plasmid pET28-Trx, separately. Second, mice were immunized with purified recombinant proteins to generate polyclonal antibody. Then we intraperitoneally injected mice bearing hepatoma 22 (H22) tumor cells to prepare antibody ascites. ELISA and Western blot were used to detect the titer and the utility of the antibody, respectively. Finally, HepG2 cells were exposed to PDGF-BB protein or anti-PDGF-B ascite antibody in different dilution concentrations groups and the proliferation of HepG2 cells was quantified by CCK8 assay. As the results, we identified mice that could produce high drop of neutralizing antibodies against hPDGF-B induced by both two recombinant proteins. Two anti-PDGF-B ascite antibodies could markedly inhibit the proliferation of HepG2 cells by blocking the stimulating effect of PDGF-BB protein. Our results suggest that Trx-PDGF-B recombinant protein as immunogen provides a new method for the preparation of PDGF-B vaccine, and also a new idea for the treatment of hepatocellular carcinoma in clinical practice.
ABSTRACT
BACKGROUND:Salvia miltiorrhiza bone-setting capsule is a traditional Chinese medicine for the treatment of fractures due to activating blood circulation to dissipate blood stasis, reducing sweling and pain. OBJECTIVE: To observe the effects of Salvia miltiorrhiza bone-setting capsule on the fracture healing in a rat model of closed femoral fractures. METHODS: Rats were randomly divided into salvia miltiorrhiza bone-setting capsule group, physiological saline group and normal group. In the salvia miltiorrhiza bone-setting capsule group and physiological saline group, rat models of closed femoral fractures were prepared, and then given physiological saline and salvia miltiorrhiza bone-setting capsule 2 pils by intragastric administration. In the normal group, rats were housed normaly. At 7, 14 and 28 days after fractures, hematoxylin-eosin staining conditions, serum osteocalcin, the expression of colagen type I, and the expression of protein and mRNA calus transforming growth factor-beta 1 were observed in the salvia miltiorrhiza bone-setting capsule group and physiological saline group. RESULTS AND CONCLUSION: (1) Hematoxylin-eosin staining demonstrated that at 7 days after fractures, no significant difference was found in pathological changes of femoral fracture in salvia miltiorrhiza bone-setting capsule group and physiological saline group. At 14 and 28 days after fractures, pathological repair was more obvious in the salvia miltiorrhiza bone-setting capsule group than in the physiological saline group. (2) At 3 and 7 days after fractures, serum osteocalcin and the expression of type I colagen were significantly increased in the salvia miltiorrhiza bone-setting capsule group and physiological saline group (P < 0.05), and the expression trend was consistent in both groups. The expression was always higher in the salvia miltiorrhiza bone-setting capsule group than in the physiological saline group, and significant differences were found at 14 and 28 days after fractures (P < 0.01). (3) Transforming growth factor beta 1 expression reached a peak at 3 days after fractures, gradualy reduced, increased at 14 days (the second peak), and diminished at 28 days in the salvia miltiorrhiza bone-setting capsule group and physiological saline group. The expression trend of transforming growth factor beta 1 was consistent in the salvia miltiorrhiza bone-setting capsule group and physiological saline group. At 7, 14 and 28 days, the transforming growth factor beta 1 expression was higher in the salvia miltiorrhiza bone-setting capsule group than in the physiological saline group. (4) Results showed that salvia miltiorrhiza bone-setting capsule could promote fracture healing, and its mechanism was probably associated with serum osteocalcin, the expression of colagen type I and transforming growth factor-β1.
ABSTRACT
Objective To retrospectively study the high risk factors for biliary complication (BC) and the application of the Clavien system to classify BC in a large cohorts of subjects undergoing liver transplantations (LT).Methods The clinical data of 181 patients who received LT from Jan.2004 to Dec.2008 were studied.BC was classified using the Clavien system.The risk factors of biliary complication were evaluated by using a binary forward stepwise logistic regression analysis.Results 14.4％ (26/181) recipients developed BC (BC group).In 84.6％ (22/26) patients the BC was above the Clavien Ⅲ b.Regression analysis of BC revealed that the placement of a T tube (P =0.0090,OR=31.177),RIld (P=0.0094,OR＜0.001).RI1w (P=0.0013,OR＞999.999) were significantly associated with the development of BC.Regression analysis of BC above Clavien Ⅲ b revealed that RIld (P=0.0065,OR＜0.001,RI1w (P=0.0022,OR＞999.999) were significantly associated with the development of BC above Clavien Ⅲ b.Conclusions The Clavien classification system was useful to classify BC.The placement of a T tube was an independent risk factor to predict BC,it was not a factor for BC above Clavien Ⅲ b.Hepatic arterial insufficiency (HAI) was an independent risk factor for BC and BC above Clavien Ⅲ b.
