Therapeutic effects of Carissa edulis aqueous extract against L-glutamic acid-induced neurotoxicity in brain mice.

卡里萨食用水提取物对L-谷氨酸诱导的小鼠脑神经毒性的治疗作用

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作者:Yadang Sabine Adeline Fanta, Nguezeye Yvette, Taiwe Germain Sotoing, Agbor Gabriel Agbor, Ngo Bum Elisabeth
The over-stimulation of N-methyl-d-aspartate glutamate receptors causes an excitotoxic neuronal death which plays an important role in many neurodegenerative diseases. Carissa edulis, a medicinal plant used in African pharmacopeia has been shown to have many therapeutic effects. In this study, the therapeutic effects of Carissa edulis aqueous extract on L-glutamic acid-induced neurotoxicity in mice were investigated. Two-month-old mice received an intraperitoneal injection of L-glutamic acid (2 g/kg) for seven consecutive days and were treated with an aqueous extract of Carissa edulis. Mice were monitored for behavioural studies including locomotion, muscle strength, and memory. Oxidative stress was determined by measuring lipid peroxidation and the level of antioxidant enzymes. Elisa kits were used to evaluate the levels of the proinflammatory cytokines. Hippocampal histopathology was examined using cresyl violet staining. Carissa edulis administration exhibited a protective effect on L-glutamic acid-induced abnormal locomotor activity and increased the mice's muscle strength. Also, it increased the memory of treated mice. Carissa edulis aqueous extract administration decreased the malondialdehyde level and increased the catalase activity and glutathione level. Furthermore, it significantly decreased the levels of IL-1β and TNF-α compared to the L-glutamic acid group. There were no significant pathological changes in the hippocampus of the Carissa edulis-treated group compared to the L-glutamic acid group. Our results indicated that Carissa edulis aqueous extract showed therapeutic effects by alleviating memory impairment, decreasing oxidative stress, and proinflammatory cytokines in the brains of mice treated with L-glutamic acid. Therefore, Carissa edulis treatment may help reduce glutamatergic neurotoxicity in neurodegenerative diseases.

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