Betulinic acid attenuates T-2 toxin-induced cytotoxicity in porcine kidney cells by blocking oxidative stress and endoplasmic reticulum stress

Li, Xiaowen; Wang, Xianglin; Liu, Sha; Ji, Wang; Liu, XiangYan; Zhu, Yuanyuan; Zhang, Linyu; Li, Rongfang

doi:10.1016/j.cbpc.2021.109124

Cited by 18 publications

(6 citation statements)

References 37 publications

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“…52 Besides, BA can regulate Ca 2+ homeostasis, as reported in some studies. 53,54 In accordance with these findings, pretreatment with BA hinders the increase in NO and Ca 2+ levels to protect against liver damage evoked by alcohol. These results indicate that BA has a protective effect on ALD, possibly by regulating ERS, which requires further investigation.…”

Section: Papersupporting

confidence: 70%

“…46,59,60 In addition, the ERinhibitory properties exhibited by BA show protective roles in some disease models, such as NAFLD and T-2 toxin-induced cytotoxicity in porcine kidney cells. 54,61 Herein, we observed a significant decrease in the protein expression of Grp78, Grp94, CHOP, and ATF6, and the phosphorylation of PERK and IRE1α in the liver after BA preprocessing. Additionally, 4-PBA could also attenuate these indices in the liver, further demonstrating that BA attenuates ALD by inhibiting ERS.…”

Section: Food and Function Papermentioning

confidence: 71%

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Suppression of endoplasmic reticulum stress-associated pathways and hepatocyte apoptosis participates in the attenuation of betulinic acid on alcohol-provoked liver injury in mice

Kong

et al. 2022

Food Funct.

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Section: Papersupporting

confidence: 70%

Section: Food and Function Papermentioning

confidence: 71%

Suppression of endoplasmic reticulum stress-associated pathways and hepatocyte apoptosis participates in the attenuation of betulinic acid on alcohol-provoked liver injury in mice

Kong

et al. 2022

Food Funct.

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“…Numerous studies have demonstrated that T2 can cause oxidative stress in various cell types, such as rat chondrocytes (Liu et al, 2021b),rat pituitary CH3 cells (Deyu et al, 2018), mouse neuroblastoma cells (Zhang et al, 2018), porcine kidney cells (Li et al, 2021), chicken heterophils (Liu et al, 2021a), and broiler hepatocytes (Yin et al, 2020). The underlying mechanism for the observed cytotoxicity, DNA damage, and apoptosis has been linked to oxidative stress (Bouaziz et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Unraveling the Nrf2-ARE Signaling Pathway in DF-1 Cells: Insights into T-2 Toxin-Induced Oxidative Stress Regulation

Yang

Gao

Xiao

et al. 2023

Preprint

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T-2 toxin (T2) poses a major threat to the health and productivity of animals and livestock. The induction of oxidative stress by T2 has been identified as a central factor in cellular damage. The Nrf2-ARE signaling pathway represents a crucial regulatory mechanism that protects cells from oxidative stress, with nuclear factor E2 related factor 2 (Nrf2) serving as a vital component in this defense. To date, there has been a lack of research on the role of Nrf2 in mediating the effects of T2-induced oxidative stress in broilers. The present study aimed to investigate the regulatory mechanism of Nrf2 protein derived from broilers against T2-induced oxidative damage by constructing Nrf2 overexpression and knockdown DF-1 cell lines. Normal DF-1 cells, Nrf2 overexpressing cells, and Nrf2 knockdown cells were subjected to treatment with 50nM T2 for 24 hours. Results showed that an increase in Nrf2 protein levels was associated with a decrease in oxidative stress in DF-1 cells (P < 0.05) and an upregulation of antioxidant factor mRNA and protein expression. Conversely, downregulation of Nrf2 protein resulted in the opposite outcomes. This study provides valuable insights into the potential treatment of oxidative stress-related diseases in livestock and poultry.

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“…It can also lead to the inhibition of protein, DNA, and RNA synthesis in animal cells, resulting in immunosuppression, oxidative stress, and apoptosis, which lead to cell damage [12]. The toxic dose of T2 in pigs is different in vivo and in vitro, just as the toxic concentration of T2 in pigs and PK15 cells is different [27,28]. Even the toxic concentration of T2 for PK15 cells and primary porcine alveolar macrophages (PAMs) of the same pig origin is different [29].…”

Section: Discussionmentioning

confidence: 99%

Low-Concentration T-2 Toxin Attenuates Pseudorabies Virus Replication in Porcine Kidney 15 Cells

Xiong

Tan

et al. 2022

Toxins

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Pseudorabies, caused by pseudorabies virus (PRV), is the main highly infectious disease that severely affects the pig industry globally. T-2 toxin (T2), a significant mycotoxin, is widely spread in food and feeds and shows high toxicity to mammals. The potential mechanism of the interaction between viruses and toxins is of great research value because revealing this mechanism may provide new ideas for their joint prevention and control. In this study, we investigated the effect of T2 on PRV replication and the mechanism of action. The results showed that at a low dose (10 nM), T2 had no significant effect on porcine kidney 15 (PK15) cell viability. However, this T2 concentration alleviated PRV-induced cell injury and increased cell survival time. Additionally, the number of PK15 cells infected with PRV significantly reduced by T2 treatment. Similarly, T2 significantly decreased the copy number of PRV. Investigation of the mechanism revealed that 10 nM T2 significantly inhibits PRV replication and leads to downregulation of oxidative stress- and apoptosis-related genes. These results suggest that oxidative stress and apoptosis are involved in the inhibition of PRV replication in PK15 cells by low-concentration T2. Taken together, we demonstrated the protective effects of T2 against PRV infection. A low T2 concentration inhibited the replication of PRV in PK15 cells, and this process was accompanied by downregulation of the oxidative stress and apoptosis signaling pathways. Our findings partly explain the interaction mechanism between T2 and PRV, relating to oxidative stress and apoptosis, though further research is required.

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Betulinic acid attenuates T-2 toxin-induced cytotoxicity in porcine kidney cells by blocking oxidative stress and endoplasmic reticulum stress

Cited by 18 publications

References 37 publications

Suppression of endoplasmic reticulum stress-associated pathways and hepatocyte apoptosis participates in the attenuation of betulinic acid on alcohol-provoked liver injury in mice

Suppression of endoplasmic reticulum stress-associated pathways and hepatocyte apoptosis participates in the attenuation of betulinic acid on alcohol-provoked liver injury in mice

Unraveling the Nrf2-ARE Signaling Pathway in DF-1 Cells: Insights into T-2 Toxin-Induced Oxidative Stress Regulation

Low-Concentration T-2 Toxin Attenuates Pseudorabies Virus Replication in Porcine Kidney 15 Cells

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