Pre-treatment but not co-treatment with vitexin alleviates hyperthermia induced oxidative stress and inflammation in buffalo mammary epithelial cells

Senthamilan, S.; Aggarwal, Anjali; Grewal, Sonika; Rani, S. Indira; Vats, Preeti; Pal, Prasanna; Jaswal, Shalini; Arya, Ashwani; Alhussien, Mohanned Naif

doi:10.1016/j.jri.2023.103979

Cited by 1 publication

(1 citation statement)

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“…A previous study by our group found that vitexin could alleviate heat stress to a certain extent in Caco-2 and Mode-k cells, and it was speculated that the antioxidant property of vitexin plays a key role in regulating heat stress [18]; however, to the best of our knowledge, the mechanism related to the modulation of heat stress by vitexin has not been previously explored. In addition, other relevant studies have confirmed that vitexin intervention alleviates high temperature-induced inflammation [19], which is mainly aimed at improving the health and productivity challenges of heat-sensitive dairy cows in the tropics. In this study, we used an in vitro cellular model to simulate the temperature and time of human heat stroke to explore the possible mechanisms of vitexin in preventing and ameliorating the possible effects of heat stress on human intestinal tract.…”

Section: Introductionmentioning

confidence: 93%

Vitexin Regulates Heat Shock Protein Expression by Modulating ROS Levels Thereby Protecting against Heat-Stress-Induced Apoptosis

Wu,

Sheng,

Tian

et al. 2023

Molecules

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Heat stress due to high temperatures can cause heat stroke, pyrexia, heat cramps, heart disease, and respiratory diseases, which seriously affect human health. Vitexin has been shown to alleviate heat stress; however, its mechanism of action remains unclear. Therefore, in this study, we used Caco-2 cells to establish a heat stress model and vitamin C as a positive control to investigate the regulatory effects of vitexin on heat-stress-induced apoptosis and the related mechanisms using Cell Counting Kit-8, flow cytometry, real-time quantitative polymerase chain reaction, and Western blot. The results showed that the mRNA expressions of Hsp27, Hsp70, and Hsp90 induced by heat stress could be effectively inhibited at vitexin concentrations as low as 30 μM. After heat stress prevention and heat stress amelioration in model cells based on this concentration, intracellular reactive oxygen species (ROS) levels and the mRNA level and the protein expression of heat shock proteins (Hsp70 and Hsp90) and apoptotic proteins were reduced. In addition, compared with the heat stress amelioration group, the expression of BCL2 mRNA and its protein (anti-apoptotic protein Bcl-2) increased in the heat stress prevention group, while the expression of BAX, CYCS, CASP3, and PARP1 mRNAs and their proteins (apoptotic proteins Bax, Cytochrome C, cle-Caspase-3, and cle-PARP1) were decreased. In summary, the heat-stress-preventive effect of vitexin was slightly better than its heat-stress-ameliorating effect, and its mechanism may be through the inhibition of intracellular ROS levels and thus the modulation of the expressions of Hsp70 and Hsp90, which in turn protects against heat-stress-induced apoptosis. This study provides a theoretical basis for the prevention and amelioration of heat stress using vitexin.

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Section: Introductionmentioning

confidence: 93%