By inhibiting pyroptosis to reduce neuroinflammation, PEG-bHb may prevent the development of secondary injury after traumatic brain injury

Abstract

Changes in severe pathological microenvironment of traumatic brain injury (TBI) have important implications for neurological repair, including oxidative stress and intense neuroinflammatory responses. Pyroptosis, a regulated cellular demise process characterized by membrane permeabilization, constitutes a primary contributor to post-traumatic brain injury induced neural inflammatory responses. Regulating the pyroptosis pathway may alleviate secondary brain injury. Polyethylene glycol-conjugated bovine hemoglobin (PEG-bHb) is a type of hemoglobin-based oxygen carriers (HBOCs) and is designed for oxygen delivery in transfusion therapy. PEG-bHb exhibits the capacity to bind and release oxygen, promoting oxygen supply in hypoxic tissues. In vivo studies have found that PEG-bHb can elevate regional oxygen saturation after TBI in prehospital stage, effectively inhibit pyroptosis, attenuate neuroinflammation and oxidative stress, and effectively attenuate the development of secondary brain injury. Furthermore, PEG-bHb has been demonstrated to protect the blood-brain barrier (BBB) by reducing the permeability of BBB and attenuating brain edema. PEG-bHb has been shown to enhance motor, learning, and memory abilities following TBI. Thus, PEG-bHb can act as a promising candidate for TBI treatment.