Abstract
Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with high disability/mortality. Baicalein has strong anti-inflammatory activity. This study aims to explore the mechanism of baicalein on brain injury after ICH. The model of brain injury after ICH was established by collagenase induction, followed by the evaluation of neurological severity, brain water content, the degenerated neurons, neuronal apoptosis, and reactive oxygen species (ROS). The ICH model was treated with baicalein or silencing NLRP3 to detect brain injury. The expression of NLRP3 inflammasome was detected after treatment with ROS scavenger. The expressions of oxidative stress markers and inflammatory factors were detected, and the levels of components in NLRP3 inflammasome were detected. Baicalein reduced the damage of nervous system, lesion surface, brain water content, and apoptosis. Baicalein inhibited malondialdehyde and increased IL-10 by inhibiting ROS in brain tissue after ICH. Baicalein inhibited the high expression of NLRP3 inflammasome in ICH. ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels. Silencing NLRP3 alleviated the brain injury after ICH by inhibiting excessive oxidative stress and inflammatory factors. Overall, baicalein alleviated the brain injury after ICH by inhibiting ROS and NLRP3 inflammasome.
Highlights
Intracerebral hemorrhage (ICH) is a cerebrovascular disease with extremely high disability and mortality rates, while existing treatments have many limitations [1, 2]
Brain water content was measured by dry/wet method, and the results showed that brain water content in ICH group was significantly increased (Fig. 1B)
These results indicated that the animal model of ICH was successfully established, and there was brain injury after ICH
Summary
Intracerebral hemorrhage (ICH) is a cerebrovascular disease with extremely high disability and mortality rates, while existing treatments have many limitations [1, 2]. A series of inflammatory responses including neuroinflammation, apoptosis and oxidative stress after ICH promote secondary brain injury after ICH, and this secondary injury is the key factor of ICH-induced brain injury [3]. Baicalein has been shown to promote neuronal and behavioral recovery after ICH by inhibiting apoptosis, oxidative stress and neuroinflammation, and can be developed as a new drug for the clinical treatment of ICH and brain injury related to ICH [3]. Baicalein reversed neuroinflammation in rats by inhibiting the NLRP3/caspase-1/Gasdermin D pathway [6]. Both the activation of NLRP3 inflammasome and reactive oxygen species (ROS) could be down-regulated by baicalein [7]. These results indicated that NLRP3 inflammasome could be inhibited by baicalein
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