Butyrolactone-I from Marine Fungal Metabolites Mitigates Heat-Stress-Induced Apoptosis in IPEC-J2 Cells and Mice Through the ROS/PERK/CHOP Signaling Pathway
2024

Butyrolactone-I from Marine Fungal Metabolites Mitigates Heat Stress in Cells and Mice

publication 10 minutes Evidence: moderate

Author Information

Author(s): Niu Xueting, Chen Shengwei, Wang Xinchen, Wen Jiaying, Liu Xiaoxi, Yong Yanhong, Yu Zhichao, Ma Xingbing, Abd El-Aty A. M., Ju Xianghong, Degl’Innocenti Donatella, Vasarri Marzia

Primary Institution: Marine Medical Research and Development Centre, Shenzhen Institute of Guangdong Ocean University

Hypothesis

Can Butyrolactone-I (BTL-I) alleviate heat-stress-induced apoptosis in intestinal cells and mice?

Conclusion

BTL-I shows potential to improve resilience to heat stress in animals by reducing apoptosis and oxidative stress.

Supporting Evidence

  • BTL-I reduced apoptosis-related protein levels in heat-stressed cells.
  • BTL-I inhibited oxidative stress markers and enhanced antioxidant activity.
  • BTL-I modulated the ROS/PERK/CHOP signaling pathway to mitigate heat stress effects.

Takeaway

This study found that a natural compound from deep-sea fungi can help protect animals from the harmful effects of heat stress.

Methodology

The study used in vitro (IPEC-J2 cells) and in vivo (mice) models to assess the effects of BTL-I on heat stress-induced apoptosis and oxidative stress.

Limitations

The study does not address the long-term effects of BTL-I or its practical application in livestock production.

Statistical Information

P-Value

p<0.01

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.3390/md22120564

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