Mechanism Study on Kaixin Powder Improving Obesity Related Cognitive Disorders in Mice
Objective To observe the improvement effect of Kaixin powder on cognitive decline in mice with obesity-related cognitive impairment model,and explore its mechanism.Methods Six-week-old C57BL/6J male mice were randomly divided into a normal diet,high-fat diet,Kaixin powder low-dose,and Kaixin powder high-dose group(10 mice in each group).The animal model of obesity-associated cognitive impairment was established by a long-term(16-week)high-fat diet,and the mice in each group were gavaged with the corresponding drugs during week 13～16 of modeling.16 weeks later,the cognitive function of mice in each group was evaluated by the Morris water maze method.After behavioral experiments,the concentrations of interleukin(IL)-6,tumor necrosis factor(TNF)-α,IL-10,and transforming growth factor(TGF)-β1 in the hippocampus were measured by ELISA.M1 and M2 microglia in the hippocampus were detected by immunofluorescence.The protein expression of Arg-1 in the hippocampus was measured by Western blot.Results Compared with normal diet mice,mice in the high-fat diet group showed a significant increase in body mass,a significant prolongation of escape latency,a significant decrease in the number of traversals across the plateau area and the exploration time of the plateau quadrant,a significant increase in the content of IL-6,TNF-α and M1 microglia in the hippocampus(P<0.01),and a significant decrease in the content of IL-10,TGF-β1,Arg-1 and M2 type microglia(P<0.01).Compared with the high-fat diet group,the mice in the Kaixin powder intervention group had decreased body mass,significantly improved cognitive function,significantly decreased IL-6,TNF-α and M1 microglia(P<0.05),and significantly increased IL-10,TGF-β1,Arg-1,and M2 microglia in the hippocampus(P<0.05).The intervention effect of Kaixin powder showed a dose-dependent effect.Conclusion Kaixin powder can reduce the level of inflammatory factors in the hippocampus by reducing body mass and regulating the conversion of microglia to M2-type in the hippocampus,and then improve the high-fat diet-induced obesity-related cognitive impairment.
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