To observe the effect of moxa smoke and cigarette smoke on hippocampal β-amyloid(Aβ) and serum inflammatory factors in APP/PS1 mice and to investigate the mechanism of moxa smoke against AD from the perspective of neuroinflammation.Methods:Thirty-six 6-month-old male APP/PS1 mice were randomized into model group，moxa smoke group，and cigarette smoke group(n=12/group)，and twelve C57BL/6 mice of the same genetic background were used as blank group.The mice in the moxa smoke and cigarette smoke groups were exposed to the moxa smoke and cigarette smoke，respectively，whose concentration was controlled within 5~15 mg/m3，while the mice in model group and blank group were exposed to normal air.The intervention time of each group was 8 weeks(20 min/day,6 days/week).Based on Congo red staining，Aβ deposition in the hippocampal tissue of mice was observed，and enzyme-linked immunosorbent assay(ELISA) was employed to detect the levels of tumor necrosis factor-α(TNF-α)，interleukin-8(IL-8)，serum amyloid A(SAA)，and C-reactive protein(CRP) in the serum of mice.Results:According to the results of Congo red staining，a large number of Aβ plaques were deposited in the model group and cigarette smoke group，and scattered Aβ particles were occasionally seen in the moxa smoke group compared with the blank group.Serum levels of TNF-α，IL-8，and CRP were higher in the model group(P<0.05) and serum levels of TNF-α，IL-8，SAA，and CRP were higher in the cigarette smoke group(P<0.05) than in the blank group.Serum IL-8 level was lower in the moxa smoke group than in the model group(P<0.05) and serum levels of TNF-α,IL-8，and CRP were lower in the moxa smoke group than in the cigarette smoke group(P<0.05).Conclusion:Moxa smoke can reduce Aβ deposition in the hippocampal region and alleviate the inflammatory response of APP/PS1 mice，suggesting that it has modulating effect on neuroinflammation in the AD brain.In addition，cigarette smoke exacerbates the development of intracranial lesions in AD patients.