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In rats fed with high-cholesterol (HC) chow, the renal specimens were investigated by microscopy and enzymehistochemistry. The levels of serum lipids, 24 h urinary protein excretion (UPE), N-acetyl-β-D-glucosaminidase (NAG) and Nitric Oxide (NO) were evaluated. Histological examination showed cell swelling, break-down and massive lipid deposition in renal tubules; perivascular and interstitial cell infiltration and mesangial cell proliferation. Enzymehistochemistry demonstrated that lactate dehydrogenase (LDH) activity in proximal tubular epithelial cells increased but succino dehydrogenase (SDH) activity decreased. The NO level in serum, urine and renal cortex were all decreased (p<0.01). Urinary NO, was negatively correlated with urinary NAG and UPE (r is -0.525, -0.529 respectively, p<0.01). This study shows that a HC diet can induce the early morphological changes in the whole kidney, particularly in the renal tubules. The decrease of NO is associated with the pathogenesis of hypercholesterolemia-induced renal injury.
In rats fed with high-cholesterol (HC) chow, the renal specimens were investigated by microscopy and enzymehistochemistry. The levels of serum lipids, 24 h urinary protein excretion (UPE), N-acetyl-β-D-glucosaminidase Histological examination showed cell swelling, break-down and massive lipid deposition in renal tubules; perivascular and interstitial cell infiltration and mesangial cell proliferation. Enzymehistochemistry of that lactate dehydrogenase (LDH) activity in proximal tubular epithelial cells increased The NO level in serum, urine and renal cortex were all decreased (p <0.01). Urinary NO, was negatively correlated with urinary NAG and UPE (r is -0.525, -0.529 respectively, p <0.01). This study shows that a HC diet can induce the early morphological changes in the whole kidney, particularly in the renal tubules. The decrease of NO is associated with the pathogenesis of hype rcholesterolemia-induced renal injury.