The Journal of pharmacy and pharmacology · 2022
p-Coumaric acid mitigates lipopolysaccharide induced brain damage via alleviating oxidative stress, inflammation and apoptosis.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Daroi Pratibha Atul, Dhage Shrikant Ninaji, Juvekar Archana Ramesh
Аннотация
OBJECTIVES: Systemic administration of lipopolysaccharide induces neuroinflammation leading to cognitive deficit and memory impairment. Herein, we investigated the effects of p-Coumaric acid (PCA) in LPS induced neuroinflammation in mice. PCA is reported to possess free radicle scavenging and neuroprotective action.
METHODS: Mice received treatment with PCA (80 mg/kg, and 100 mg/kg, p.o.) for 28 days. LPS (0.25 mg/kg) was administered intraperitoneally from Day 15 to 21, to all groups. Memory impairment and cognitive deficit were assessed by MWM and Y maze test, followed by estimation of ROS, TNF-α, IL-6, caspase-3 and c-Jun in the brain homogenate by ELISA. Histopathological changes were investigated using Nissl and H&E staining.
KEY FINDINGS: PCA attenuated increased oxidative stress, significantly increasing SOD, GSH levels and decreasing MDA level and AChE activity in mice brain, lowered the levels of TNF-α and IL-6 indicating protection against neuroinflammatory reaction. PCA also suppressed neuronal apoptosis, as indicated by decreased levels of caspase-3 and c-Jun. Further, histopathological findings revealed that PCA attenuated neuronal loss and pathological abnormalities in the hippocampus.
CONCLUSIONS: Our findings give compulsive evidence suggesting a protective effect of PCA in neuroinflammation, cognitive impairment and neuronal apoptosis induced by LPS, through its antioxidant, AChE inhibitory, anti-inflammatory and antiapoptotic activity determined by behavioural, biochemical and histopathological measures.
METHODS: Mice received treatment with PCA (80 mg/kg, and 100 mg/kg, p.o.) for 28 days. LPS (0.25 mg/kg) was administered intraperitoneally from Day 15 to 21, to all groups. Memory impairment and cognitive deficit were assessed by MWM and Y maze test, followed by estimation of ROS, TNF-α, IL-6, caspase-3 and c-Jun in the brain homogenate by ELISA. Histopathological changes were investigated using Nissl and H&E staining.
KEY FINDINGS: PCA attenuated increased oxidative stress, significantly increasing SOD, GSH levels and decreasing MDA level and AChE activity in mice brain, lowered the levels of TNF-α and IL-6 indicating protection against neuroinflammatory reaction. PCA also suppressed neuronal apoptosis, as indicated by decreased levels of caspase-3 and c-Jun. Further, histopathological findings revealed that PCA attenuated neuronal loss and pathological abnormalities in the hippocampus.
CONCLUSIONS: Our findings give compulsive evidence suggesting a protective effect of PCA in neuroinflammation, cognitive impairment and neuronal apoptosis induced by LPS, through its antioxidant, AChE inhibitory, anti-inflammatory and antiapoptotic activity determined by behavioural, biochemical and histopathological measures.