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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 1, January/February 2020

AFRICA

31

and functional damage in the heart.

2

The accumulation of ROS

activated Nrf2 during exhaustive exercise, but did not produce

a sufficient level of activation to prevent oxidative damage, and

drugs were required to further activate Nrf2. Nrf2 was expressed

at significantly higher levels after the Sal treatment. However, the

expression of Nrf2 mRNA was not affected by Sal, indicating

that Sal did not regulate Nrf2 expression at the transcriptional

or translational level, but instead at the post-translational level.

According to Numazawa, inducers rarely promote the

biosynthesis of Nrf2.

25

The epigenetic regulation of Nrf2 activity

might involve a long-term or basic regulatory mechanism. Sal

may either inhibit Keap1 expression or promote its degradation.

The abundance of Nrf2 was inhibited and its degradation was

reduced, increasing the level of Nrf2 protein. The level of Nrf2

in the nucleus increased significantly as the concentration of Sal

increased. Sal induced nuclear translocation of Nrf2.

Devling

et al.

used an siRNA to antagonise the Keap1

mRNA and its expression decreased significantly. The authors

observed a significant increase in the level of Nrf2 transported

to the nucleus. Moreover, the levels of antioxidant enzymes were

also increased significantly.

26,27

The antioxidant enzyme system downstream of Nrf2 consists

of SOD, CAT and GSH and plays a role in preventing cardiac

remodelling and cardiac function disorders.

28,29

In the control

group, a positive correlation was observed between EDPVR and

GSH, while dP/dt

max

and GSH were positively correlated in the

ES group. Therefore GSH exerted a protective effect on the heart

and improved cardiac function parameters.

The observed decrease in levels of GSH and other enzymes

after exhaustive exercise was due to their function in reversing

ROS levels. The levels of SOD, CAT and GSH all increased with

increasing concentrations of Sal. Sal induced Nrf2 expression

and increased levels of downstream antioxidant enzymes by

increasing the amount of Nrf2 protein and activating its nuclear

translocation.

Conclusion

Sal protected the heart from exhaustive exercise-induced injury,

and it may improve cardiac function and cardiac bioelectricity

in exhausted rats. Sal improved the antioxidant capacity by

activating Nrf2.

This study was supported by grants from the Medical Science Research

Programme of the Chinese Army (CWS12J064), the Medical Technology

Project of the Chinese Army (BWS11J058), the Logistical Science Research

Project of the Chinese Army (CBJ13J002), the National Natural Science

Foundation of China (81870249), and the National Key R&D Programme of

China (2017YFC0908700 and 2017YFC0908703).

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