Neuroimmunomodulation · 2021
Scopoletin Attenuates Intracerebral Hemorrhage-Induced Brain Injury and Improves Neurological Performance in Rats.
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Zhang Wanzeng, Zhao Wangmiao, Ge Chunyan, Li Xiaowei, Sun Zhaosheng
Аннотация
BACKGROUND: Among the hypertension-related complications, the onset of intracerebral hemorrhage (ICH) is a destructive stage and is the most disabling type of stroke that has the highest death rate. At present, there is no promising treatment for ICH.
OBJECTIVES: The present investigation was aimed at evaluating the safeguarding effect of scopoletin against ICH-induced brain injury.
METHODS: We used Wistar male rats and divided them into 4 groups. Group 1 served as control, group 2 was induced with ICH, group 3 served as scopoletin-pretreated ICH rats, and group 4 as scopoletin drug control. During the experimental period, neurobehavioral outcome, cerebral edema, and neuroinflammation parameters were evaluated using RT-PCR and other biochemical analyses.
RESULTS: The rats that received scopoletin treatment demonstrated a significant attenuation in neurological deficits, neurodegeneration markers expression (TREM-1, SERPINE-1), and restored cerebral edema compared to ICH animals. On the other hand, an upsurge in inflammatory cytokines, for example, TNF-α, IL-13, IL-1β, and IL-17, was observed in ICH rats and was reduced to the level near normalcy in the scopoletin-treated groups.
CONCLUSION: Our investigations propose that the effectiveness of scopoletin in improving acute neurological function after ICH is promising, and this could be a lead molecule for the development of treatment plans in ICH treatment.
OBJECTIVES: The present investigation was aimed at evaluating the safeguarding effect of scopoletin against ICH-induced brain injury.
METHODS: We used Wistar male rats and divided them into 4 groups. Group 1 served as control, group 2 was induced with ICH, group 3 served as scopoletin-pretreated ICH rats, and group 4 as scopoletin drug control. During the experimental period, neurobehavioral outcome, cerebral edema, and neuroinflammation parameters were evaluated using RT-PCR and other biochemical analyses.
RESULTS: The rats that received scopoletin treatment demonstrated a significant attenuation in neurological deficits, neurodegeneration markers expression (TREM-1, SERPINE-1), and restored cerebral edema compared to ICH animals. On the other hand, an upsurge in inflammatory cytokines, for example, TNF-α, IL-13, IL-1β, and IL-17, was observed in ICH rats and was reduced to the level near normalcy in the scopoletin-treated groups.
CONCLUSION: Our investigations propose that the effectiveness of scopoletin in improving acute neurological function after ICH is promising, and this could be a lead molecule for the development of treatment plans in ICH treatment.