Oxidative Stress Damage In Mice Research Articles

Protective Effect of Que Zui Tea on d-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway.

Que Zui tea (QT) is an important herbal tea in the diet of the 'Yi' people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6'-O-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6'-O-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.

Erdosteine prevents contrast-induced renal oxidative stress damage in mice

Purpose: To investigate the protective effect of erdosteine on contrast-induced renal oxidative stress in mice.
 Methods: C57BL/6 mice were injected intraperitoneally with contrast medium to establish an acute kidney injury model (AKI). Renal function, blood urea nitrogen (BUN) and serum creatinine (SCr) were determined. Also, oxidative stress, lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) were evaluated. And the renal tissue structure was examined by light microscopy, while Western blot (WB) and Real-time polymerase chain reaction (RT-PCR) were used to determine the expressions of senescence-related factor, Nrf-2 and downstream antioxidant factor.
 Results: Erdosteine improved the renal structure of mice and significantly decreased serum BUN and SCr levels. In addition, erdosteine promoted the expression of antioxidant enzymes SOD1, SOD2, GPX1 and GPX3 in renal tissues, decreased the content of ROS, and inhibited the content of LDH and MDA in serum. Also, WB and RT-PCR results showed that erdosteine activated Nrf2 pathway, thereby alleviating contrast-induced renal injury.
 Conclusion: Erdosteine inhibits contrast-induced renal oxidative stress in mice and delays cell senescence by activating Nrf2 pathway. This will be of great significance in the treatment of contrast-induced nephropathy.