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  • Title: [Effect of telmisartan on tubulointerstitial injury and expression of PPARγ in rat renal tissue of IgA nephropathy model].
    Author: Xing L, Bai L, Yu CY, Xie RJ.
    Journal: Zhonghua Yi Xue Za Zhi; 2010 Nov 02; 90(40):2860-3. PubMed ID: 21162800.
    Abstract:
    OBJECTIVE: To observe the effect of telmisartan on the expression of PPARγ in rat renal tissue of IgA nephropathy model and clarify the possible mechanism of telmisartan in tubulointerstitial injury. METHODS: The experimental rat model with IgA nephropathy was induced by bovine serum albumin (BSA), lipopolysaccharide (LPS) and carbon tetrachloride (CCl4). Forty male SD rats were randomly divided into control group, IgA model group, rosiglitazone group, telmisartan group and losartan group. At pre-administration, Weeks 4, 8 and 10, the quantity of 24-hour proteinuria was measured. The morphologic changes of renal tissues were evaluated by electron microscope. Immunohistochemistry was used to observe the expressions of PPARγ, TGF-β1 and α-smooth muscle actin (α-SMA) in different groups and RT-PCR to detect the expressions of PPARγ, TGF-β1 and monocyte chemoattractant protein-1 (MCP-1) in different groups. RESULTS: Compared with control group, 24-hour proteinuria(mg) increased markedly in IgA model group (14.14 ± 1.99 vs 1.59 ± 0.18), but rosiglitazone group (2.35 ± 0.33), telmisartan group (1.88 ± 0.09) and losartan group (2.82 ± 0.34) was much lower and telmisartan had the most significant effect (all P < 0.05). Compared with control group, there were varying degrees of mesangial proliferation and infiltration of inflammatory cell in IgA model group (3.10 ± 0.18). The tubulointerstitial injury was notably alleviated in rosiglitazone group (1.97 ± 0.23), telmisartan group (1.57 ± 0.14) and losartan group (2.15 ± 0.22) while telmisartan had the most significant effect (all P < 0.01). With immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), PPARγ, TGF-β1, α-SMA and MCP-1 had minimal expression on tubule and interstitium in normal group. But there was a high expression in model group. There was no difference between losartan and model groups. There was a lowered expression in rosiglitazone and telmisartan groups. CONCLUSION: Possibly through two separate passway of stimulating PPARγ and preventing Angiotensin II receptor, telmisartan shows special protective function in tubulointerstitial injury.
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