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논문분류	춘계학술대회 초록집
제목	Paricalcitol has the Renoprotective Effect Related to Catalase Pathway in Kidney Injury
저자	Young Sun Kang1, Jeong Yeon Gee1, Jeong Eun Kim1, Hye Sook Min1, Seong Jin Kim1,Ji Eun Lee2, Hyun Wook Kim2, Dae Ryong Cha1
출판정보	2014; 2014(1):
키워드	카탈라제, 비타민 D, 당뇨병성 신증, 산화스트레스
초록	Wongang University Sanbon Hospital, Department of Nephrology2 Background: Paricalcitol, vitamin D receptor agonist, is known to play an antioxidative role in tissue injury. Recently catalase overexpression or deficiency mice model have showed interesting results of its antioxidative role in several reports. However, there is no data for the roles of paricalcitol in the diabetic complication related to them of catalase. Therefore, we investigated the effect of paricalcitol on the oxidative stress of diabetic nephropathy in catalase knock-out diabetic mice. Methods: 8-week-old catalase knock-out (CKO) C57/BL6 mice and wild-type (WT) mice were treated by intraperitoneal streptozotocin (50 mg/kg/day) injection for 7 days. After inducing of diabetes, they were treated by intraperitoenal paricalcitol injection for two months. They were grouped into follows: I) WT 2) CKO 3) CKO+paricalcitol 4) WT+STZ 5) WT+STZ+Paricalcitol 6) CKO+STZ 7) CKO+STZ+Paricalcitol. Result: Body weight, blood pressure, heart rate, fasting blood glucose level were not significant among groups. Organ weights and urinary volume were also similar among groups. However, interestingly, urinary albumin excretion was more increased in CKO than WT mice and reduced significantly by paricalcitol treatment. These changes were also observed in STZ-induced diabetic mice. Gene expressions of MCP-1, IL-10, TGFβ and type Ⅳ collagen were inhibited by paricalcitol treatment in diabetic CKO mice. These results were consistent with protein expressions of TGFβ and PAI-1 by western blot analysis and immunohistochemistry. In addition, HbA1c, glucose tolerance test, and insulin tolerance test were of interest significantly improved by paricalcitol treatment in diabetic CKO mice. However, both lipid contents and liperoxidase of kidney tissue were reduced only in non-diabetic CKO mice by paricalcitol, but not in diabetic CKO mice. In addition, urinary 8-isoprostane level was also dramatically decreased in non-diabetic CKO mice by paricalcitol, but which did not induce any change in diabetic CKO mice. Conclusion: Altogether, these results suggest that the kidney injury associated with catalase deficiency was improved paricalcitol treatment in both diabetic and non-diabetic nephropathy. However, paricalcitol has the renoprotective effect through independent of the antioxidative role of catalase in diabetic nephropathy. Further study should be investigated about them.
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