Mild hypothermia regulates neuronal inflammation and oxidative stress through HSP70 to alleviate brachial plexus injury.

OBJECTIVE

To investigate the function of mild hypothermia (MH) in brachial plexus injury (BPI) by regulating the 70 kDa heat shock protein (HSP70).

METHODS

A BPI model mouse was established to investigate the mechanism of MH and HSP70 on BPI through hematoxylin-eosin staining, enzyme-linked immunosorbent assay (ELISA), dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining, and western blotting assays. A cellular model was established by stimulating the motor neuron-like cell line NSC-34 cells with lipopolysaccharide (LPS). The effects of MH and HSP70 on LPS-induced NSC-34 cell proliferation, cytokines, apoptosis, and oxidative stress were studied using western blotting, cell counting kit-8, ELISA, and DCFH-DA staining.

RESULTS

MH treatment inhibited the expression of HSP70 in the brachial plexus tissues of BPI mice, reduced levels of pro-inflammatory cytokines and oxidative stress, and diminished the apoptosis in neural tissues. Knockdown of HSP70 further promoted the protective effects of MH on BPI mice. Cell experiments indicated that MH treatment alleviated the inhibitory effect of LPS on the proliferation of NSC-34 cells by inhibiting HSP70 protein expression, while also reducing reactive oxygen species, oxidative stress, and apoptosis rates.

CONCLUSIONS

MH has protective effects on BPI mice by downregulating HSP70 level, inhibiting cellular oxidative stress and apoptosis.