Ascorbic acid deficiency accelerates aging of hepatic stellate cells with up-regulation of PPARγ

Il-Hwa Hong¹, Jung-Youn Han¹, Moon-Jung Goo¹, Sung-Young Hwa², Mi-Ran Ki¹, Jin-Kyu Park¹, Kyung-Sook Hong¹, Ok-Kyung Hwang¹, Tae-Hwan Kim¹, Sung-Eun Yoo³ and Kyu-Shik Jeong<sup>1

1</sup>Department of Pathology, College of Veterinary Medicine, Kyungpook National University, Daegu, Republic of Korea, ²Jinju Bio Food, Jinju and ³Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea.

Offprint requests to: Prof. Kyu-Shik Jeong, D.V.M., PhD., Department of Pathology, College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea. e-mail: jeongks@knu.ac.kr


Summary. Senescent cells have been observed in certain aged or damaged tissues. However, the information about the effects of aging on liver cells is limited. In the present study, we have examined age-related histological changes in the livers of senescence marker protein knockout (SMP30^-/-) mice, which are considered as a murine aging model due to the more sensitive response to apoptotic reagents and due to their shorter life span. In livers of old SMP30^-/- mice, numerous hepatic stellate cells (HSCs) were hypertrophic and contained abundant microvesicular lipid droplets in cytoplasm. We have found that the expression of peroxisome proliferators-activated receptor γ (PPARγ), which is a protein related to lipid metabolism and HSC quiescence, was increased in hypertrophic HSCs by aging and vitamin C (VC) deficiency, whereas these phenomena were dramatically reduced by antioxidant treatment. Therefore, these prominent phenotypic changes can be considered as aging markers in the livers of animals which are subjected to antioxidant property evaluation. Histol Histopathol 27, 171-179 (2012)

Key words: SMP30 knockout mice, Aging, Ascorbic acid, PPARγ, Hepatic stellate cells, Hypervitaminosis A

DOI: 10.14670/HH-27.171