ABSTRACT
<p><b>OBJECTIVE</b>To explore the correlation between pathological characteristics of target organs and excess evil syndrome in IgA nephropathy.</p><p><b>METHODS</b>Data were collected in multicenter cooperation. Totally 266 IgA nephropathy patients were typed into exogenous wind-heat affection syndrome (49 cases), lower energizer damp-heat syndrome (100 cases), damp-phlegm syndrome (43 cases), and blood stasis syndrome (74 cases). Meanwhile, percutaneous renal biopsy was performed in all patients for Hass classification, Oxford classification, Katafuchi integral, and Jiang's classification methods. The correlation between excess evil syndrome and pathological index was analyzed.</p><p><b>RESULTS</b>Four syndrome types were correlated with their Hass levels (r = 0. 341, P <0. 01). Affection of exogenous wind-heat syndrome was correlated with segmental proliferation of endothelial cells and damaged active lesions of segmental capillary loops. Lower-energizer damp-heat syndrome was associated with Hass III level, destroying active lesions of capillary loops, segmental proliferation of endothelial cells, glomerular segmental lesions, focal interstitial infiltration of inflammatory cells, focal interstitial fibrosis and tubular atrophy. Blood stasis syndrome was associated with Hass IV level, glomerular sclerosis, segmental glomerulosclerosis (S)/adhesion, mesangial hypercellularity (M), angiohyalinosis, multi-foci interstitial infiltration of inflammatory cells, multi-foci interstitial fibrosis and tubular atrophy. Phlegm-damp syndrome had higher proportions of Hass I and III levels, but with no association with other pathological parameters.</p><p><b>CONCLUSIONS</b>Excess evil syndrome was associated with partial pathological characteristics of IgA nephropathy. It could reflect pathological damage degree of target organs, activities, chronic lesions, and prognosis of IgA nephropathy to certain extent. Correlated pathological characteristics and its evolution could indicate excess evil syndrome types and their evolution rules.</p>
Subject(s)
Humans , Capillaries , Fibrosis , Glomerulonephritis, IGA , Pathology , Glomerulosclerosis, Focal Segmental , Kidney Glomerulus , Medicine, Chinese Traditional , Prognosis , SyndromeABSTRACT
Objective To study the effect of adenovirus type 3I,7b on the expressions of mRNA and protein of transforming growth factor-beta 1(TGF-?1) in human embryonic lung fibroblast cells.Method The expression of mRNA and protein of TGF-?1 were determined in human embryonic lung fibroblast cells before and after being infected by adenovirus type 3I,7b and in normal fibroblast cells with enzyme-linked immunosorbent assay and in situ hybridization.Results The mRNA and protein of TGF-?1 expression in human embryonic lung fibroblast cells increased siginificantly after being infected by adenovirous type 3I,7b compared with those in normal fibroblast cells(Pa0.05).Conclusion Lung fibroblast cells and TGF-?1 may play some roles in pathophysiological processes of viral pneumonia.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of qingfei oral liquid (QOL) contained serum on protein expression of transforming growth factor-beta1 (TGF-beta1) and platelet derived growth factor-BB (PDGF-BB) of adenovirus type 3I, 7b induced human embryonic lung fibroblast cells.</p><p><b>METHODS</b>The cells were divided into 5 groups, the normal cells group (NCG), the virus control group (VCG), the blank serum group (BSG), the ribavirin group (RVG) and the QOL contained serum group (QSG). All the cells except those in the NCG were challenged by adenovirus type 3I, 7b and treated with correspondent medicine. The contents of TGF-beta1 and PDGF-BB in the supernatant of cell culture were monitored by ELISA and compared among groups.</p><p><b>RESULTS</b>Contents of TGF-beta1 and PDGF-BB in VCG were significantly higher, while those in QSG were significantly lower than those in VCG (P < 0.01).</p><p><b>CONCLUSION</b>Adenovirus infection can increase the protein expression of TGF-beta1 and PDGF-BB of human embryonic lung fibroblast cells. QOL can decrease the protein expression of these cytokines, which maybe one of the mechanisms of its antiviral effect.</p>