OBJECTIVE: To study the change of levels of plasma heat stress protein 70 (HSP70) and cytokine and their interrelationship in pathogenicity of heat apoplexy. METHODS: Plasma HSP70 was determined with Western blot, and plasma interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R) and interleukin-6 (IL-6) were determined with enzyme-linked immunosorbent assay (ELISA). RESULTS: Plasma level of HSP70 was 4 211.2 +/- 1,286.2 (integral optical density) in average in the patients of heat apoplexy group, 4,137.8 +/- 1, 207.5 in those of severe heat apoplexy group, and 6,043.5 +/- 1,354.8 in control group, with very significant difference (P < 0.01). Plasma IL-2 level was (64.3 +/- 32.3) pg/ml and (200.0 +/- 50.0) pg/ml and sIL-2R (54.9 +/- 33.3) U/ml and (167.5 +/- 89.0) U/ml in the patients with heat apoplexy and in controls, respectively, with very significant difference. But, there was no significant difference in IL-6 between varied groups. CONCLUSIONS: The above-mentioned results suggest that establishment of heat acclimatization correlates to the interaction of network of neuroendocrine-cytokine-HSP, in which decrease in plasma IL-2 was one of the important factors causing reduction of HSP70 expression. Balance of network regulation was broken by pathological factors, finally resulting in heat apoplexy.
OBJECTIVE: To study the change of levels of plasma heat stress protein 70 (HSP70) and cytokine and their interrelationship in pathogenicity of heat apoplexy. METHODS: Plasma HSP70 was determined with Western blot, and plasma interleukin-2 (IL-2), soluble interleukin-2 receptor (sIL-2R) and interleukin-6 (IL-6) were determined with enzyme-linked immunosorbent assay (ELISA). RESULTS: Plasma level of HSP70 was 4 211.2 +/- 1,286.2 (integral optical density) in average in the patients of heat apoplexy group, 4,137.8 +/- 1, 207.5 in those of severe heat apoplexy group, and 6,043.5 +/- 1,354.8 in control group, with very significant difference (P < 0.01). Plasma IL-2 level was (64.3 +/- 32.3) pg/ml and (200.0 +/- 50.0) pg/ml and sIL-2R (54.9 +/- 33.3) U/ml and (167.5 +/- 89.0) U/ml in the patients with heat apoplexy and in controls, respectively, with very significant difference. But, there was no significant difference in IL-6 between varied groups. CONCLUSIONS: The above-mentioned results suggest that establishment of heat acclimatization correlates to the interaction of network of neuroendocrine-cytokine-HSP, in which decrease in plasma IL-2 was one of the important factors causing reduction of HSP70 expression. Balance of network regulation was broken by pathological factors, finally resulting in heat apoplexy.