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, administered orally) for 8 weeks. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and creatinine (Cr) in the serum were tested. Histopathological features were assessed by hematoxylin and eosin (HE) staining followed by an assessment of the antioxidant and anti-inflammatory activities. Furthermore, we also evaluated the expression levels of the genes Bax, Bcl-2 and cleaved caspase-3 in the liver and kidney. The results showed that Uro A treatment obviously attenuated d-gal-induced liver and kidney damage. The beneficial effects of Uro A were accompanied by a decline in malondialdehyde (MDA) levels and a rise in the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and total antioxidant capacity (T-AOC) activity in the liver and kidney and downregulation of the levels of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), in serum. Moreover, Uro A could modulate the expression of Bax, Bcl-2 and cleaved caspase-3 in the livers and kidneys of aging mice. These findings suggested that Uro A ameliorated d-gal-induced liver and kidney injury through attenuating oxidative stress, inflammatory responses and apoptosis.
Chen et al. (2020) studied this question.