Abstract
A previous study from our team found that hyperbaric oxygen (HBO) pretreatment attenuated decompression sickness (DCS) spinal cord injury by upregulating heat shock protein 32 (HSP32) via the ROS/p38 MAPK pathway. Meanwhile, a MEK1/2-negative regulatory pathway was also activated to inhibit HSP32 overexpression. The purpose of this study was to determine if normobaric oxygen (NBO) might effectively induce HSP32 while concurrently inhibiting MEK1/2 and to observe any protective effects on spinal cord injury in DCS rats. The expression of HSP32 in spinal cord tissue was measured at 6, 12, 18, and 24 h following NBO and MEK1/2 inhibitor U0126 pretreatment. The peak time of HSP32 was observed at 12 h after simulated air diving. Subsequently, signs of DCS, hindlimb motor function, and spinal cord and serum injury biomarkers were recorded. NBO-U0126 pretreatment significantly decreased the incidence of DCS, improved motor function, and attenuated oxidative stress, inflammatory response, and apoptosis in both the spinal cord and serum. These results suggest that pretreatment with NBO and U0126 combined can effectively alleviate DCS spinal cord injury in rats by upregulating HSP32. This may lead to a more convenient approach for DCS injury control, using non-pressurized NBO instead of HBO.
Highlights
Decompression sickness (DCS) is caused by inert gas bubbles forming in tissues and vessels following inadequate decompression in diving, aviation, and space activities (Vann et al, 2011)
The factorial design analysis showed that neither normobaric oxygen (NBO) nor U0126 alone impacted on heat shock protein 32 (HSP32) expression (P > 0.05), but NBO and U0126 had a positive interaction on HSP32 upregulation in the NBO-U0126 treatment group (P < 0.001, Figure 2B)
Neither NBO nor U0126 alone had a significant impact on DCS incidence (P > 0.05), and no treatment made a significant difference to the latency or proportion of mortality in rats (P > 0.05)
Summary
Decompression sickness (DCS) is caused by inert gas bubbles forming in tissues and vessels following inadequate decompression in diving, aviation, and space activities (Vann et al, 2011). NBO-U0126 on DCS SCI after active treatment, and more than 20% sequelae remain afterward (Blatteau et al, 2011; Mahon and Regis, 2014; Saadi et al, 2019). By increasing blood oxygen partial pressure and extending oxygen diffusion, HBO accelerates inert gas washout and attenuates hypoxic and ischemic damage caused by bubbles in tissues (Arieli et al, 2009). While upregulating the expression of HSP32 in spinal cord neurons, HBO activated the MEK1/2-negative regulatory pathway to prevent HSP32 overexpression (Huang et al, 2016). As an important effector of HBO, moderately expressed HSP32 exerts antioxidative, anti-inflammatory, and antiapoptotic effects, while overexpressed HSP32 results in numerous inimical effects (Schipper et al, 2019)
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