Weiyue Jin1, Yurun Xue1, Yucong Xue2, Xue Han2, Qiongtao Song3, Jianping Zhang1, Ziliang Li1, Jie Cheng4, Shengjiang Guan5, Shijiang Sun6, Li Chu7. 1. School of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050200, Hebei, China. 2. School of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, Hebei, China. 3. Ophthalmopathy Prevention & Cure and Visual Function Protection With TCM Laboratory, Chengdu 610075, Sichuan, China. 4. Affiliated Hospital, Hebei University of Chinese Medicine, Shijiazhuang 050011, Hebei, China. 5. School of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050200, Hebei, China; Affiliated Hospital, Hebei University of Chinese Medicine, Shijiazhuang 050011, Hebei, China. Electronic address: guanshengjiang123@126.com. 6. Affiliated Hospital, Hebei University of Chinese Medicine, Shijiazhuang 050011, Hebei, China. Electronic address: sunshijiang6909@163.com. 7. School of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang 050200, Hebei, China; Hebei Key Laboratory of Integrative Medicine on Liver-Kidney Patterns, Shijiazhuang 050200, Hebei, China. Electronic address: chuli0614@126.com.
Abstract
BACKGROUND AND PURPOSE: Tannic acid (TA), a group of polyphenolic compounds, has multiple anticancer, antimutagenic, antioxidant and anti-inflammatory activities. However, the effects of TA on arsenic trioxide (ATO)-induced nephrotoxicity are still relatively unknown. This study investigated the protective effects and potential mechanisms of TA on ATO-induced nephrotoxicity in rats. METHODS: Rats were intragastrically administered TA with concurrent ATO infused intraperitoneally over 10 days. Renal morphology changes were observed through light microscopy. The levels of antioxidants and pro-inflammatory factors were measured in the serum and renal tissue, respectively. Further, expression of B-cell lymphoma-2, B-cell lymphoma-extra large, p53, and Bcl-2-associated X protein were measured using an immunohistochemical method. The protein expression of nuclear factor kappa B (NF-κB), nuclear factor-erythroid-2-related factor 2 (Nrf2), and kelch-like ECH-associated protein 1 (Keap1) were measured by Western blot. RESULTS: The data showed that ATO exposure significantly increased the serum nephritic, oxidative stress, apoptosis and inflammatory markers in the renal tissue of rats. Conversely, pretreatment with TA reversed these changes. Furthermore, TA treatment caused a significant decrease in NF-κB expression (P < 0.05), while increasing Nrf2 and Keap1 expressions (P < 0.05). CONCLUSION: TA ameliorates ATO-induced nephrotoxicity, which is related to the inhibition of oxidative stress, inflammation and apoptosis, potentially through the NF-κB/Nrf2 pathway.
BACKGROUND AND PURPOSE:Tannic acid (TA), a group of polyphenolic compounds, has multiple anticancer, antimutagenic, antioxidant and anti-inflammatory activities. However, the effects of TA on arsenic trioxide (ATO)-induced nephrotoxicity are still relatively unknown. This study investigated the protective effects and potential mechanisms of TA on ATO-induced nephrotoxicity in rats. METHODS:Rats were intragastrically administered TA with concurrent ATO infused intraperitoneally over 10 days. Renal morphology changes were observed through light microscopy. The levels of antioxidants and pro-inflammatory factors were measured in the serum and renal tissue, respectively. Further, expression of B-cell lymphoma-2, B-cell lymphoma-extra large, p53, and Bcl-2-associated X protein were measured using an immunohistochemical method. The protein expression of nuclear factor kappa B (NF-κB), nuclear factor-erythroid-2-related factor 2 (Nrf2), and kelch-like ECH-associated protein 1 (Keap1) were measured by Western blot. RESULTS: The data showed that ATO exposure significantly increased the serum nephritic, oxidative stress, apoptosis and inflammatory markers in the renal tissue of rats. Conversely, pretreatment with TA reversed these changes. Furthermore, TA treatment caused a significant decrease in NF-κB expression (P < 0.05), while increasing Nrf2 and Keap1 expressions (P < 0.05). CONCLUSION:TA ameliorates ATO-induced nephrotoxicity, which is related to the inhibition of oxidative stress, inflammation and apoptosis, potentially through the NF-κB/Nrf2 pathway.
Authors: Manish Mishra; Larry Nichols; Aditi A Dave; Elizabeth H Pittman; John P Cheek; Anasalea J V Caroland; Purva Lotwala; James Drummond; Christy C Bridges Journal: Int J Mol Sci Date: 2022-09-21 Impact factor: 6.208