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Carnosic acid prevents heat stress-induced oxidative damage by regulating heat-shock proteins and apoptotic proteins in mouse testis

  • 0College of Veterinary Medicine, 70578 Nanjing Agricultural University , Nanjing, 210095, China.
Biological Chemistry +

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December 4, 2024

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December 4, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Carnosic acid protects male fertility from heat stress by preserving testicular structure and testosterone levels. Its benefits in wild-type mice were linked to modulating heat shock and apoptosis proteins, unlike in knockout mice.

Area Of Science

  • Reproductive Biology
  • Biochemistry
  • Oxidative Stress Research

Background

  • Heat stress negatively affects male reproductive health in livestock and humans.
  • Carnosic acid (CA) is a potent antioxidant with demonstrated protective effects against oxidative stress and apoptosis.
  • Alpha B-crystallin (αB-crystallin) is a small heat shock protein involved in regulating apoptosis and oxidative stress.

Purpose Of The Study

  • To investigate the protective role of Carnosic acid (CA) against heat-induced testicular damage.
  • To determine if the protective effects of CA are dependent on the presence of αB-crystallin.

Main Methods

  • Utilized wild-type and αB-crystallin knockout mice subjected to controlled heat stress.
  • Administered Carnosic acid (CA) as a pretreatment before heat exposure.
  • Assessed testicular structure, testosterone levels, and the expression of heat shock proteins (Hsp27, Hsp70) and cleaved caspase-3.

Main Results

  • CA pretreatment significantly increased testosterone levels and maintained testicular structure in wild-type mice under heat stress.
  • In contrast, CA showed no protective effect on testicular parameters in αB-crystallin knockout mice.
  • CA administration reduced levels of Hsp27, Hsp70, and cleaved caspase-3 in wild-type mice, whereas cleaved caspase-3 levels increased in knockout mice.

Conclusions

  • Carnosic acid (CA) demonstrates significant protective effects on the male testis against heat stress, particularly in the presence of αB-crystallin.
  • The findings suggest that CA's protective mechanism involves the modulation of heat shock proteins and apoptosis-related pathways, potentially mediated by αB-crystallin.
  • This study highlights the potential of CA as a therapeutic agent for mitigating reproductive dysfunction caused by heat stress.

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