Tetramethylpyrazine Attenuates the Endotheliotoxicity and the Mitochondrial Dysfunction by Doxorubicin via 14-3-3γ/Bcl-2

Figure 9

Diagram exhibiting a new mechanism of TMP protects mitochondrial function via 14-3-3γ/Bcl-2 in Dox-induced endotheliotoxicity. Dox induced excessive mitochondrial ROS generation, activating RIRR mechanism, weakening MMP, opening mPTP, induce ROS burst, leading to mitochondrial dysfunction, which in turn damages vascular endothelium. TMP upregulated 14-3-3γ expression of vascular endothelium, promoted the translocation of Bcl-2 into mitochondria, closed mPTP, keeped MMP, inhibited RIRR mechanism, thereby suppressed oxidative stress, improved mitochondrial function, and alleviated Dox-induced endotheliotoxicity.