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KMID : 0811720130170050435
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Korean Journal of Physiology & Pharmacology
2013 Volume.17 No. 5 p.435 ~ p.440
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Antiapoptotic Effect of Paricalcitol in Gentamicin-induced Kidney Injury
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Suh Sang-Heon
Lee Ko-Eun
Park Jeong-Woo
Kim In-Jin
Kim Ok
Kim Chang-Seong
Choi Joon-Seok
Bae Eun-Hui
Ma Seong-Kwon
Lee Jong-Un
Kim Soo-Wan
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Abstract
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While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 ?g/kg/day) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynu-cleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.
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KEYWORD
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Apoptosis, Gentamicin, Kidney, Paricalcitol
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