3.2 Heat stress and LPS triggered HPMEC apoptosis via activating
endothelial glycocalyx degradation
Changes in ultrastructure and apoptosis of HPMEC The
ultrastructure of HPMEC was next observed to estimate the effects of
heat stress and LPS om HPMEC apoptosis (Figure 2A ). Normal
cellular structures were observed in CON group. In model groups, cells
tended to generate characteristics of apoptosis such as swollen, broken
membranes, abnormal organelles including nucleus, mitochondria and
endoplasmic reticulum (Figure 2A ). Cells assigned to HPSE were
more obvious but cells assigned to UFH were milder than HS+LPS group
(Figure 2A ). These results suggested that an altered structure
in HPMEC as a result of stimulation of heat stress and LPS.
Evidence suggested that heat stress may lead to cellular apoptosis,23 we next analyzed HPMEC activities through flow
cytometry using Annexin V-FITC/PI staining. As expected, assignment of
HPMEC with heat stress and LPS increased apoptotic rates in both HPSE
and UFH treatment, compared with CON group (P < 0.05)
(Figure 2B,C ). This increase is more pronounced in HPSE group
(P < 0.05) (Figure 2B,C ), suggesting potential
effects of damaged glycocalyx on HPMEC apoptosis.