&lt;p&gt;Protective role of quercetin against manganese-induced injury in the liver, kidney, and lung; and hematological parameters in acute and subchronic rat models [Retraction]&lt;/p&gt;

Bahar, Entaz; Lee, Geum-Hwa; Bhattarai, Kashi Raj; Lee, Hwa Young; Kim, Hyun-Kyoung; Handigund, Mallikarjun; Choi, Min‐Kyung; Han, Sunyoung; Chae, Han‐Jung; Yoon, Hyonok

doi:10.2147/dddt.s207534

Cited by 2 publications

(1 citation statement)

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“…Our findings suggested that Cd induced hepatocyte apoptosis through oxidative stress, so an antioxidant was urgently needed to alleviate the oxidative damage caused by Cd exposure. QE is a natural organic antioxidant ( Bahar et al, 2019 ), It can reportedly counteract Cd-induced neurotoxicity in rat brain, significantly improve Cd-induced abnormalities in biochemical and histological indicators ( Prabu et al, 2010 ), and inhibit Cd-induced autophagy in mouse kidneys ( Yuan et al, 2016 ). In the current work, after QE intervention, the contents of ALT, AST, and LDH in the supernatant of culture medium were reduced, and the damage inflicted by Cd to hepatocytes decreased.…”

Section: Discussionmentioning

confidence: 99%

Alleviating effect of quercetin on cadmium-induced oxidative damage and apoptosis by activating the Nrf2-keap1 pathway in BRL-3A cells

Wang

Ding

et al. 2022

Front. Pharmacol.

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Cadmium (Cd) is a toxic heavy metal extensively used in industrial and agricultural production. Among the main mechanisms of Cd-induced liver damage is oxidative stress. Quercetin (QE) is a natural antioxidant. Herein, the protective effect of QE on Cd-induced hepatocyte injury was investigated. BRL-3A cells were treated with 12.5 μmol/L CdCl2 and/or 5 μmol/L QE for 24 h. The cells and medium supernatant were collected, and the ALT, AST, and LDH contents of the medium supernatant were detected. The activities or contents of SOD, CAT, GSH, and MDA in cells were determined. Intracellular ROS levels were examined by flow cytometry. Apoptosis rate and mitochondrial-membrane potential (ΔΨm) were detected by Hoechst 33,258 and JC-1 methods, respectively. The mRNA and protein expression levels of Nrf2, NQO1, Keap1, CytC, caspase-9, caspase-3, Bax, and Bcl-2 were determined by real-time PCR (RT-PCR) and Western blot methods. Results showed that Cd exposure injured BRL-3A cells, the activity of antioxidant enzymes decreased and the cell ROS level increased, whereas the ΔΨm decreased, and the expression of apoptotic genes increased. Cd inhibited the Nrf2-Keap1 pathway, decreased Nrf2 and NQO1, or increased Keap1 mRNA and protein expression. Through the combined action of Cd and QE, QE activated the Nrf2-Keap1 pathway. Consequently, antioxidant-enzyme activity decreased, cellular ROS level decreased, ΔΨm increased, Cd-induced BRL-3A cell damage was alleviated, and cell apoptosis was inhibited. After the combined action of QE and Cd, Nrf2 and NQO1 mRNA and protein expression increased, Keap1 mRNA and protein expression decreased. Therefore, QE exerted an antioxidant effect by activating the Nrf2-Keap1 pathway in BRL-3A cells.

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Section: Discussionmentioning

confidence: 99%