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Войти в исследования Advanced biomedical research · 2026
Barbaloin Attenuates Cerebral Ischemia and Reperfusion Injury in Rats and Inhibits Lipopolysaccharide-Stimulated Inflammatory Responses in BV2 Microglial Cells.
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Liu Caiyun, Wang Lin, Ren Hongyan, Liu Lijun, Yang Zhihu
Аннотация
BACKGROUND: Barbaloin (BAR) is a naturally occurring bioactive anthracycline derived from the leaf exudates of aloe plants with a variety of biological and pharmacological properties. The aim of the present study was to investigate the neuroprotective effects of BAR against cerebral ischemia and reperfusion (I/R) injury in rats and the possible underlying mechanisms.
MATERIALS AND METHODS: Middle cerebral artery occlusion followed by reperfusion was used to induce cerebral I/R injury in rats, and BAR was administered intraperitoneally after the onset of ischemia.
RESULTS: We found that BAR remarkably improved neurological scores, reduced brain infarct volume, and inhibited neuronal apoptosis in cerebral I/R rats. Furthermore, BAR upregulated Bcl-2 protein levels and downregulated cleaved caspase-3, Bax, and inducible nitric oxide synthase (iNOS) in the ischemic cortex. I/R injury-induced increases in malondialdehyde content, and decreases in glutathione, glutathione peroxidase, and superoxide dismutase activities were significantly attenuated by BAR administration. In vitro, BAR pretreatment inhibited the release of proinflammatory cytokines (iNOS, tumor necrosis factor-α, and interleukin-6) and reduced protein levels of iNOS and nuclear expression of nuclear factor-κB p65 in lipopolysaccharide-stimulated BV-2 microglial cells.
CONCLUSION: Taken together, our data suggest that BAR possesses neuroprotective effects against cerebral I/R injury through antiapoptotic, antioxidative, and anti-inflammatory properties.
MATERIALS AND METHODS: Middle cerebral artery occlusion followed by reperfusion was used to induce cerebral I/R injury in rats, and BAR was administered intraperitoneally after the onset of ischemia.
RESULTS: We found that BAR remarkably improved neurological scores, reduced brain infarct volume, and inhibited neuronal apoptosis in cerebral I/R rats. Furthermore, BAR upregulated Bcl-2 protein levels and downregulated cleaved caspase-3, Bax, and inducible nitric oxide synthase (iNOS) in the ischemic cortex. I/R injury-induced increases in malondialdehyde content, and decreases in glutathione, glutathione peroxidase, and superoxide dismutase activities were significantly attenuated by BAR administration. In vitro, BAR pretreatment inhibited the release of proinflammatory cytokines (iNOS, tumor necrosis factor-α, and interleukin-6) and reduced protein levels of iNOS and nuclear expression of nuclear factor-κB p65 in lipopolysaccharide-stimulated BV-2 microglial cells.
CONCLUSION: Taken together, our data suggest that BAR possesses neuroprotective effects against cerebral I/R injury through antiapoptotic, antioxidative, and anti-inflammatory properties.