【Animal Modeling】-The neuroprotective effect of artesunate on mice with experimental autoimmune encephalomyelitis and the effect of autophagy

  Objective: How to study the neuroprotective and autophagy effects of artesunate on experimental autoimmune encephalomyelitis (EAE) mice?

  Method: Do you want to randomly select 48 female C57BL/6 mice in the blank group? There are four groups of models: artesunate low-dose and high-dose groups, each with 12 animals. The MOG35-55 peptide was used to create an EAE model. Artesunate low-dose and high-dose groups received artesunate (10 mg). /(Kg?D), 50mg/(kg?D)) intraperitoneal injection, for 10 consecutive days, have you observed seizures in mice? The brain tissue was stained with Luxol Fast Blue (LFB) and demyelination was observed, and it was passed Western blotting-I? How to detect the expression of autophagy-related proteins LC3 and LC3-II?

  Result: None of the mice in the blank group were affected by the disease. Do the mice in the model group also have the disease? Do the artesunate mice in each dose group have different degrees of sagging, unsteady gait, and hindlimb weakness? Compared with the model group, the incubation period of each dose group of artesunate was reduced, the peak period was delayed, and the neurological function score was reduced. The low-dose group of the high-dose group had a significant effect (P0.05). (2) LFB staining showed that the myelin sheath of the model group was loosely arranged. Is the myelin staining of each artesunate treatment group damaged, faded and improved? (3) Compared with the blank group of the Western blot detection model group, the optical density of LC3-I, LC3-II band and LC3-II/LC3-I ratio, and the optical density of LC3I to LC3II band and LC3-Artemisia annua The ratio of II/LC3-I of each dose group of succinate decreased (P\u003c 0.01). Is there a significant effect in the high-dose group and the low-dose group (P\u003c0.05)?

  Conclusion: Artesunate has a neuroprotective effect on EAE mice and can reduce the demyelination of brain tissue. Its mechanism of action is LC3-I? Does downregulation of LC3-II and LC3-II/LC3-I reduce autophagy?