Context
Bazi Bushen capsule (BZBS) has anti-ageing properties and is effective in enhancing memory.
Objective
To find evidence supporting the mechanisms and biomarkers by which BZBS functions.
Materials and methods
Male C57BL/6J mice were randomly divided into five groups: normal, ageing, β-nicotinamide mononucleotide capsule (NMN), BZBS low-dose (LD-BZ) and BZBS high-dose (HD-BZ). The last four groups were subcutaneously injected with
d
-galactose (
d
-gal, 100 mg/kg/d) to induce the ageing process. At the same time, the LD-BZ, HD-BZ and NMN groups were intragastrically injected with BZBS (1 and 2 g/kg/d) and NMN (100 mg/kg/d) for treatment, respectively. After 60 days, the changes in overall ageing status, brain neuron morphology, expression of p16
INK4a
, proliferating cell nuclear antigen (PCNA), ionized calcium-binding adapter molecule 1 (Iba1), postsynaptic density protein 95 (PSD95), CD11b, Arg1, CD206, Trem2, Ym1 and Fizz1, and the senescence-associated secretory phenotype (SASP) factors were observed.
Results
Compared with the mice in the ageing group, the HD-BZ mice exhibited obvious improvements in strength, endurance, motor coordination, cognitive function and neuron injury. The results showed a decrease in p16
INK4a
, Iba1 and the upregulation of PCNA, PSD95 among brain proteins. The brain mRNA exhibited downregulation of Iba1 (
p
< 0.001), CD11b (
p
< 0.001), and upregulation of Arg1 (
p
< 0.01), CD206 (
p
< 0.05), Trem2 (
p
< 0.001), Ym1 (
p
< 0.01), Fizz1 (
p
< 0.05) and PSD95 (
p
< 0.01), as well as improvement of SASP factors.
Conclusions
BZBS improves cognitive deficits via inhibition of cellular senescence and microglia activation. This study provides experimental evidence for the wide application of BZBS in clinical practice for cognitive deficits.