3.3 Heat stress and LPS activated vWF, ET-1, E-selectin, VCAM-1,
and Occludin released in HPMEC
To further investigate the effect of heat stroke on the function of
coagulation factors, the expression of vWF and ET-1 was assessed under
stimulation of heat stress and LPS. Exposure to stimulation of heat
stress and LPS resulted in a statistically significant increase in the
expression of vWF and ET-1 (P < 0.05) (Figure
3A ). HPSE treatment significantly increased generation of vWF and ET-1,
but The generation of vWF and ET-1 was significantly increased by HPSE
treatment but was reduced by UFH treatment in comparison with HS+LPS
treatment alone. These results indicated that heat stress and LPS
directly affect glycocalyx degradation as a potential mechanism to
induce clotting state in HPMEC.
Given previous studies indicating the importance of VCAM-1 and
E-selectin in forecasting cellular inflammation 24 and
the critical role of Occludin in preventing endothelial leakage,25, 26 in this study, we also aimed to examine the
expression of VCAM-1, E-selectin, and Occludin. Our results showed that
heat stress and LPS significantly enhanced the expression of VCAM-1 and
E-selectin but attenuated Occludin expression in comparison with the CON
group (P < 0.05) (Figure 3B,C ). Compared with
HS+LPS treatment alone, HPSE treatment significantly upregulated the
production of VCAM-1 and E-selectin, but downregulated Occludin
expression. This data suggested that heat stress and LPS destructed the
tight junctions between endothelial cells and aggravated endothelial
leakage in HPMEC.