Inflammopharmacology · 2026
Yucca filamentosa extract therapeutic potential against neuro-inflammation and demyelination through modulation of eicosanoids.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Ullah Malik Saad, Asghar Areej, Chauhdary Zunera, Irfan Muhammad, Afzal Samina
Аннотация
BACKGROUND: Multiple sclerosis is a chronic inflammatory disease characterized by the demyelination of nerve cells. So, it is mandatory to find out such phytochemicals that may prove to be helpful in treating neurodegeneration. Yucca filamentosa possesses anti-inflammatory, antioxidant and healing properties for the damaged neurons.
METHOD: Yucca filamentosa extract (YFE) was prepared and GCMS fingerprinting and molecular docking was performed. Animals divided as Normal, Demyelination disease model, Standard care group, and three treatment groups as YFE 250 mg/kg, 500 mg/kg and 750 mg/kg. Cuprizone 0.2% was mixed in chow diet to induce multiple sclerosis for 42 days.
RESULTS: GC-MS profiling indicates the presence of oleic acid, phytol, and thymol. Neurobehavioral studies were carried out after YFE treatment. Cuprizone caused motor dysfunction as well as anxiety-like behavior in rats. Treatment groups showed notable improvement in the function of motor neurons, and cognition in behavioral tests. YFE downregulated mRNA expression of TNFα, IL-6, ABPP, Alpha synuclein, and acetylcholinesterase. YFE also decreased serum level of TNF-α, IL-6, PGE2, Nitric oxide, myeloperoxidase and leukotrienes B4 in treatment groups.
CONCLUSION: YFE exhibited neuroprotective potential through inhibition of oxidative stress, inflammation and modulation of neurodegenerative markers.
METHOD: Yucca filamentosa extract (YFE) was prepared and GCMS fingerprinting and molecular docking was performed. Animals divided as Normal, Demyelination disease model, Standard care group, and three treatment groups as YFE 250 mg/kg, 500 mg/kg and 750 mg/kg. Cuprizone 0.2% was mixed in chow diet to induce multiple sclerosis for 42 days.
RESULTS: GC-MS profiling indicates the presence of oleic acid, phytol, and thymol. Neurobehavioral studies were carried out after YFE treatment. Cuprizone caused motor dysfunction as well as anxiety-like behavior in rats. Treatment groups showed notable improvement in the function of motor neurons, and cognition in behavioral tests. YFE downregulated mRNA expression of TNFα, IL-6, ABPP, Alpha synuclein, and acetylcholinesterase. YFE also decreased serum level of TNF-α, IL-6, PGE2, Nitric oxide, myeloperoxidase and leukotrienes B4 in treatment groups.
CONCLUSION: YFE exhibited neuroprotective potential through inhibition of oxidative stress, inflammation and modulation of neurodegenerative markers.