ABSTRACT
Objective To investigate podocyte number, the expression of nephrin and transforming growth factor-β1(TGF-β1) in adriamycin-induced-nephropathy rat model and its significance. Methods The rat adriamycin nephrosis model was constructed to detect blood and urine biochemical indicators and observe the pathological changes of renal tissues by light microscope and electron microscope. The expression levels of nephrin and TGF-β1 as well as the podocyte number were examined at different time points by immunohistochemistry. Results The pathological changes of the renal tissues were obvious. Nephrin presented a weak signal at the end of the first week (P<0.05). TGF-β1 started to increase (P<0.05) while the podocyte number started to decrease at the end of the eighth week (P<0.05). Expression of nephrin was negatively correlated with the P<0.05) and serum creatinine (r=-0.71, P<0.05). Expression of TGF-β1 was blood urea nitrogen (r=0.62, P<0.05) and serum creatinine (r=0.59, urinary protein (r=-0.63, P<0.05), blood urea nitrogen (r=-0.72, P<0.05) and serum creatinine (r=-0.76, P<0.05); it was positively correlated with nephrin (r=0.78, P<0.01) but negatively correlated with TGF-β1 (r=-0.64, P<0.05). Conclusion The acute and chronic adriamycin nephrosis models were twice every two weeks. The genesis and development of proteinuria are closely related to the abnormal expression of nephrin. Focal segmental glomerulosclerosis occurs when the podocyte number decreases and TGF-β1 accelerates it.
ABSTRACT
Objective To study the adriamycin nephrosis model in different development pathological stages. Methods The rat adriamycin nephrosis model was established by injecting adriamycin into tail-vein twice every two weeks to detect blood and urina biochemical indicators and to observe the pathological changes of the renal tissues. Results The model showed serious edema,proteinuria,hypoproteinemia,and hyperlipidemia. Podocytes were swollen and mesangial cells developed mild hyperplasia at the end of the fourth week. The nephric tubule atrophied at the end of the eighth week accompanied with adhesion between glomeruli and Bowman's capsule. Glomeruli sclerosis of mild or medium degree was observed at the end of the twelfth week with obvious lymphocyte infiltration in the renal interstitium as well as the formation of collagen fibers. Conclusion The adriamycin nephrosis model was successfully developed by injecting adriamycin 4 mg/kg into tail-vein twice every two weeks. The acute model is similar to human minimal change disease,and the chronic model is similar to human focal segmental glomerulosclerosis.
ABSTRACT
Objective To investigate podocyte number,the expression of nephrin and transforming growth factor-?1(TGF-?1) in adriamycin-induced-nephropathy rat model and its significance.Methods The rat adriamycin nephrosis model was constructed to detect blood and urine biochemical indicators and observe the pathological changes of renal tissues by light microscope and electron microscope.The expression levels of nephrin and TGF-?1 as well as the podocyte number were examined at different time points by immunohistochemistry.Results The pathological changes of the renal tissues were obvious.Nephrin presented a weak signal at the end of the first week(P
ABSTRACT
Objective To study the protective effect of glucocorticoid preconditioning on the myocardial ischemic and reperfused hearts.Methods Totally 18 rabbits were randomly divided into three groups: myocardial ischemia-reperfusion model(model),high-dose glucocorticoid given by one time group(high-dose group) and low-dose glucocorticoid given by several times group(low-dose group),with six rabbits in each group.Myocardial ischemia was induced by left anterior descending coronary artery ligation.ST segments were recorded by the BL-420 biological signal acquisition system.Plasma malondial dehyde(MDA) was examined before ischemia,at 15 min after ischemia and 30 min after reperfusion;ischemic heart muscles were prepared with cryotomy and stained histochemically.Succinic dehydrogenase activity was observed in the ischemic region.Results There was shorter time of ST-segment recovery in the high-dose group and the low-dose group than that in the model group.Serum level of MDA in the high-dose group was lower than in the low-dose group(P
ABSTRACT
Objective To observe the morphological changes of corneal nerve in experimental herpes simplex keratitis (HSK) in rabbit eyes. Methods Inoculation of the scarified cornea with herpes simplex virus-Ⅰ(HSV-Ⅰ)leads to herpetic infection of cornea. The HSK was detected by slit lamp and polymerase chain reaction(PCR), and the changes of corneal nerves in various periods with methylene blue vital staining and ultrastructure of corneal nerve were studied. Results Under light microscope, fewer corneal nerve bundles were observed, scattered with lower density of nerve fiber at center of cornea on the 4th day after the infection. At days 7 and 14, the seriously damaged nerve fiber was intermittent. The neuraxon became shorter with little polarity and the density of nerve fiber was extremely low. At day 30, the density was still low while the nerve fiber was approximately normal. Under electromicroscope, at day 4, the lamellar sheath of nerve fiber in the epitheliums appeared intermittent, and the neuroplasm of endings was partly lysed. During day 7 to day 14,neuroplasm was damaged and became vacuolar. The mitochondria swelled with vacuolar crest, and then were destroyed and lysed. The nerves in stroma were also injured. On day 30, neurilemma sheath was still intermittent with the decrease of microfilament and racuole. Conclusion HSK leads to the damage of nerve and the decrease of nerval density, and the damage of corneal nerve repairs very slowly.