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Objective To investigate the mechanism of pulmonary inflammation induced by influenza virus , and provide reference for the development of effective drugs for viral pneumonia .Methods An influenza PR8 infection mouse model was established .The levels of inflammatory cytokines and complement molecules were determined using RT -PCR and ELISA.The pathological changes were examined using biopsy .The complement inhibitor cobra venom factor ( CVF) was injected intraperitoneally at a dose of 50 μg/( kg· 24 h) , and then body mass .The survival rate and inflammatory factors were examined .Results Compared with the control group , the expressions of complement regulatory molecule Crry and CD59 were significantly decreased (P<0.01), while those of complement C9 and complement receptor C3aR and C5aR were significantly increased in the lungs of influenza model mice (P<0.01).Pro-inflammatory cytokines TNF-α, IL-6 and IFN-γwere highly expressed , but anti-inflammatory cytokine IL-2 was lowly expressed in serum .Treatment with CVF caused a sight body mass loss, a survival rate increase and a lung index decrease (P <0.05).Moreover, an IL-2 expression increase and a decrease of IL-6, TNF -αand INF-γexpression were observed in CVF treatment mice ( P< 0.05).Conclusion Inhibition of complement activation can increase the survival rate of mice with influenza pneumonia and decrease pulmonary indexes .thus delaying the pathogenesis of PR 8.
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Aim To study the development of acute lung inflammation in mice induced by activation of the complement alternative pathway and the changes of the related indicators, and to provide an ideal pathological model of acute lung inflammation in mice for drug screening and intervention. Methods Cobra venom factor( CVF) was used to activate complement alterna-tive pathway of SPF Kunming mice by intravenous injection. According to different sampling time, the mice were divided into 15 min, 30 min, 1 h, 2 h, 6 h group, and the parallel PBS control groups were set at the same time. Lung coefficient, lung water content, myeloperoxidase ( MPO ) activity, BALF cell number and protein content were tested. The pathological changes of lung tissue were observed by HE staining. The concentration of IL-6 , TNF-α, P-selectin and ICAM-1 in bronchoalveolar lavage fluid ( BALF ) and serum were determined by ELISA. Results CVF caused pulmonary inflammatory cell infiltration in mice obviously. Compared with PBS groups, MPO activity of lung tissue, BALF cell and the protein concentration were significantly increased. The contents of IL-6, TNF-α, P-selectin in BALF and serum were in-creased, and the content of ICAM-1 in serum was also increased. The content of P-selectin in BALF reached the first peak at 30 min point, the content of IL-6 and TNF-α in BALF reached the first peak at 1 h point, but the indicators had no further changes at 2 h point, and all the indicators rose again at 6 h point. The lev-els of IL-6 and TNF-α in serum reached peak at 1 h point,then the content showed lower levels at the sub-sequent time points. The levels of P-selectin and ICAM-1 in serum increased along the time. Lung coef-ficient, lung water content and ICAM-1 of the BALF showed no significant alteration. Conclusion The ac-tivation of the complement alternative pathway can lead to acute lung inflammation in mice and the inflammato-ry response is the most obvious at 30 min to 1 h. The study could provide an ideal pathological model of a-cute lung inflammation in mice for drug screening and intervention.
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The purpose of this study is to evaluate the variation of radiation dose distribution for liver tumor located in liver dome and for the interest organs(normal liver, kidney, stomach) with the pencil beam convolution (PBC) algorithm versus anisotropic Analyticalal algorithm (AAA) of the Varian Eclipse treatment planning system, The target volumes from 20 liver cancer patients were used to create treatment plans. Treatment plans for 10 patients were performed in Stereotactic Body Radiation Therapy (SBRT) plan and others were performed in 3 Dimensional Conformal Radiation Therapy (3DCRT) plan. dose calculation was recalculated by AAA algorithm after dose calculation was performed by PBC algorithm for 20 patients. Plans were optimized to 100% of the PTV by the Prescription Isodose in Dose Calculation with the PBC algorithm. Plans were recalculated with the AAA, retaining identical beam arrangements, monitor units, field weighting and collimator condition. In this study, Total PTV was to be statistically significant (SRS: p=0.018, 3DCRT: p=0.006) between PBC and AAA algorithm. and in the case of PTV, ITV in liver dome, plans for 3DCRT were to be statistically significant respectively (p=0.013, p=0.024). normal liver and kidney were to be statistically significant (p=0.009, p=0.037). For the predictive index of dose variation, CVF ratio was to be statistically significant for PTV in the liver dome versus PTV (SRS r=0.684, 3DCRT r=0.732, p<0.01) and CVF ratio for Tumor size was to be statistically significant (SRS r=-0.193, p=0.017, 3DCRT r=0.237, p=0.023).
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Humanos , Rim , Fígado , Neoplasias Hepáticas , Compostos Organotiofosforados , Características da População , PrescriçõesRESUMO
Objective: To explore the mechanism of congestive heart failure (CHF) by observing the effects of Tingli Shengmai Decoction on myocardial fibrosis and expression of TGF-?1 of rats with CHF. Methods: The CHF animal models were duplicated by the abdomen arteriarctia method, and 60 male wistar rats were randomly divided into the sham-operation group, the model group, the high-dose of Tingli Shengmai Decoction group, the low-dose of Tingli Shengmai Decoction group and the positive medicine (Xinbaowan) control group. After 4 weeks common fed, every group rats were given a certain dose of distilled water or medicine. After 8 weeks, hemodynamic parameters were detected, MASSON staining was used in the study of collagen type in left ventricular interstitial tissue, collagen volume fraction (CVF) were measured by image analysis, and expression of TGF-?1 in myocardium were evaluated by immunohistochemical staining. Results: Compared with the sham-operated group, CVF of model control group increased significantly (P
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Aim To investigate the effect of 3,3′,4′,5,7-pentamethylquercetin(PMQ) on angiotensin Ⅱ(AngⅡ) induced cardiac fibrosis.Methods Thirty rats were randomly assigned to the 5 groups,6 each:① control group: Saline was administrated daily via gavage for 21 days;② PMQ group: PMQ(50 mg?kg-1) was administrated daily via gavage for 21 days;③ AngⅡ group: AngⅡ(288 ?g?kg-1?d-1)was injected subcutaneously daily from the 15 th day;④ PMQ+ AngⅡ group: PMQ and AngⅡ were administrated as above;and ⑤ solvent+ AngⅡ group: Solvent and AngⅡ were administrated as above.After the rats were euthanized on the 22 nd day,the myocardial hydroxyproline content,SOD activity and MDA content were measured,and the expression of collagenⅠ,collagenⅢ,and NADPH oxidase subunits Nox2 and p47phox mRNA were determined by real time-PCR.Collagen volume fraction(CVF) Ⅰand Ⅲ were detected by immunohistochemistry,and CVFⅠ/CVFⅢ was calculated.Results PMQ reduced cardiac fibrosis in AngⅡ induced hypertension rats by decreasing the myocardial hydroxyproline content,downregulating the expression of collagenⅠand collagenⅢ mRNA,and decreasing CVFⅠ,CVFⅠ/CVFⅢ.PMQ exerted antioxidant function by increasing SOD activity and decreasing MDA content and reducing the mRNA expression of NADPH oxidase subunits Nox2 and p47phox.Conclusion PMQ could reduce cardiac fibrosis,which may result from the inhibition of the expression of NADPH oxidase.The results suggest that PMQ may represent a promising therapeutic approach for CHF treatment.