Figure 10. The mechanism of myocardial cell apoptosis caused by mechanical trauma.

Patients with systemic mechanical trauma present intestinal barrier dysfunction, causing intestinal bacteria translocation and the release of toxins into the blood, resulting in a significant increase in the level of LPS in plasma. LPS, as a powerful inflammation factor, can activate monocytes, and enhance the expression of TNF-α gene, causing the abnormal increase of TNF-α. And increased TNF-α in plasma can induce overexpression of iNOS/NADPH oxidase, resulting in massive production of O₂⁻ and superoxide anions in myocardial tissues. Consequently, oxidative stress reaction causes damage to the heart, resulting in secondary cardiac insufficiency after mechanical trauma. The current experiments showed that after GSPE interference, the content of TNF-α from monocytes stimulated by LPS had decreased significantly, as well as the content of inflammatory indicator TNF-α in plasma after mechanical trauma. Meanwhile, GSPE can also effectively inhibit excessive ROS production from myocardial cells and block oxidative stress. Furthermore, the degree of increased Ca²⁺ concentration in cardiomyocytes stimulated by plasma after mechanical trauma was significantly declined in GSPE interference group, and myocardial cell’s calcium overload was significantly mitigated (as shown in red arrows).