ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of geniposide on treating experimental CP rats.</p><p><b>METHOD</b>The animal model of CP was made with rats by injecting hemorrhoid injection. Rats in experiment group were randomly devided into model group, Qianliekang tablets group (2 g x kg(-1)) and geniposide high, middle, low dose groups (20, 10, 5 mg x kg(-1)). Subsequently, the state of all rats, prostate index, WBC and lecithine corpuscle, LDH5/LDH1, and prostatic histopathological changes were observed. Count of total cellular score (TCS) and quantitation of inflammatory cell, fibroblasts, glandular organ, calculation of glandular cavity area, and their changes of morphology were analyzed.</p><p><b>RESULT</b>Compared with model group, the prostate index, WBC and LDHS/LDH1 of the rats in Qianliekang tablets group, high dose geniposide group and middle dose geniposide group were significantly decreased, while the quantities of lecithine corpuscle were remarkably increased (P < 0.01 or P < 0.05). Compared with model group, the number of inflammatory cells and fibroblasts in Qianliekang tablets group, high dose geniposide group were decreased, and the quantity of glandular organ and area of glandular cavity in these groups were increased (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Geniposide of high and middle dose can reduce leucocytes infiltration, restrain the hyperplasia of fibrous tissue, and recover the secretion function of prostate. It show that geniposide is significantly potential to cure rats which are exposed to chronic prostatitis.</p>
Subject(s)
Animals , Male , Rats , Body Weight , Chronic Disease , Drug Therapy , Disease Models, Animal , Dose-Response Relationship, Drug , Iridoids , Pharmacology , Therapeutic Uses , Isoenzymes , Metabolism , L-Lactate Dehydrogenase , Metabolism , Leukocyte Count , Prostate , Metabolism , Pathology , Prostatitis , Blood , Drug Therapy , Pathology , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To study the effect of geniposide-acid(GA) on the anti-inflammatory action for adjuvant-induced arthritis (AA) rats and the proliferation of synoviocytes in AA rats and the feasible mechanism of apoptosis in vitro.</p><p><b>METHOD</b>Forty-eight health male Wistar rats were divided randomly into six groups and were administered respectively with 200, 100, 50 mg x kg(-1) GA and 0.75 mg x kg(-1) MTX and normal sodium (normal or model control group) for four weeks when right posterior paw pads of rats excluding normal control group were injected intrademally with complete Freund's adjuvant after 19 days. The left posterior paws swelling degree, swelling inhibition ratio and arthritis index of secondary inflamation were detected. The TNF-alpha and IL-1beta proteins in serum of rats were assayed by enzyme linked immunosorbent assay (ELISA) kits. The synovial fibroblasts of AA rats were exposed to 1-4 micromol x L(-1) GA or 4 micromol x L(-1) MTX. The effect of GA on the proliferation of synoviocytes was detected by MTT assay. The morphologic change of apoptosis cells was observed by Hoechst/PI double stainning and fluorescence microscope. The rate of apoptosis cells was analyzed by flow cytometry. The mRNA expresstion of Bcl-2 and Bax gene was detected by reverse transcription PCR (RT-PCR).</p><p><b>RESULT</b>200 mg kg(-1) or 100 mg kg(-1) GA could decrease significantly the paw swelling degree, arthritis index and the level of TNF-alpha and IL-1beta proteins in serum of AA rats (P < 0.05 or P < 0.01) with 25.4%, 21.37% of the swelling inhibition ratio respectivly, 34.61%, 28% of protein inhibition ratio of TNF-alpha and 29.05%, 21.65% of that of IL-1beta. GA(1-4 micromol x L(-1)) inhibitated significantly the proliferation of synoviocytes culcured for 5 days. Flow cytometry showed that 1, 2, 4 micromol x L(-1) GA increased obviously the rate of apoptosis cells, the apoptosis ratios were 15.8%, 24.3%, 40.7% respectivly (P < 0.01). RT-PCR showed GA could decrease the expression level of Bcl-2 gene but increase that of Bax gene (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>GA could inhibit the secondary inflamation of AA rats and decrease the level of TNF-alpha and IL-1beta protein in the AA rats serum. GA could inhibit the proliferation of AA rat synoviocytes in vitro and induce apoptosis which mechanism was concerned with down-regulating the mRNA expression of Bcl-2 and up-regulating that of Bax.</p>
Subject(s)
Animals , Humans , Male , Rats , Anti-Inflammatory Agents , Apoptosis , Arthritis, Experimental , Drug Therapy , Allergy and Immunology , Cytokines , Allergy and Immunology , Disease Models, Animal , Freund's Adjuvant , Glucosides , Iridoid Glucosides , Iridoids , Random Allocation , Rats, Wistar , Synovial Fluid , Cell Biology , Allergy and ImmunologyABSTRACT
Aim To investigate the protective effects and mechanism of astragaloside Ⅳ on hypertrophy induced by angiotensinⅡ(AngⅡ)in primary cultured cardiomyocytes of neonatal rats.Methods Cardiomyo-cytes were incubated with AngⅡ to establish the hypertrophy model of primary cultured cardiomyocytes in neonatal rats.AST 10 mg?L-1 or 20 mg?L-1 were added with AngⅡ simultaneously to observe its protective effects on cardiomyocytes.The diameter and the total protein content of cardiomyocyte were measured.The intracellular free calcium concentration([Ca2+]i),activity of sarcoplasmic reticulum Ca2+-ATPases(SERCA)and activity of calcineurin(CaN)were determined.Results Compared with control group,diameter and total protein content of cardiomyocyte induced by AngⅡ were increased significantly,which were inhibited by AST 10 mg?L-1 and 20 mg?L-1,respectively(P
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AIM To study the effect of Gardenia jasminoides Ellis on serum IL-1? and TNF-? level of rheumatoid arthritis rats, as well as its mechanism. METHODS An experimental type Ⅱ collagen-induced arthritic rats was established. The inhibitory effects on paw edema were observed, and serum IL-1? and TNF-? levels were determined in experimental rats. RESULTS Compared with models, Gardenia jasminoides Ellis inhibited paw edema on rats significantly, and the levels of serum IL-1? and TNF-? showed markedly decrease by Gardenia jasminoides Ellis at high dose to medium dose( P
ABSTRACT
AIM To study the protective effects of vesnarinone on myocardial ischemia. METHODS Rat myocardial oxide nitric (NO) content, protein kinase C (PKC) activities in different groups were determined by kits. RESULTS Vesnarinone 1 mg?kg -1 or 2 mg?kg -1 iv markedly improved the NO content and PKC activity before ischemia for 30 min and reperfusion for 2 h in rats. CONCLUSION Vesnarinone possesses a protective effect against myocardial ischemia via NO induce PKC.