Effects of saponins from Panax japonicus on neuronal apoptosis of natural aging rats by NLRP1 and NLRP3 inflammasome pathway / 中草药
Zhongcaoyao
; Zhongcaoyao;(24): 4941-4945, 2017.
Article
en Zh
| WPRIM
| ID: wpr-852355
Biblioteca responsable:
WPRO
ABSTRACT
Objective To observe the effects of saponins from Panax japonicus on neuronal apoptosis of natural aging rats and its mechanisms based on NLRP1 and NLRP3 inflammasome pathway. Methods Male SD rats in a SPF grade were randomly divided into five groups: control group (9-month-old rats), model group (24-month-old rats), and SPJ treatment group (10, 30, and 60 mg/kg). From the beginning of 18 months, animals were treated with SPJ (or normal saline) by ig until 24 months, and stopped 2 d each week for six months of continuous administration. The neural apoptosis situation of cortex and hippocampus in aging rats were observed by TUNEL method. The protein expression of IL-1β, ASC, NLRP3, NLRP1, Caspase-1, and IL-18 of the cerebral cortex and hippocampal were detected by Western blotting. Results TUNEL results showed that there were a very small number of apoptotic cells in the cortex and hippocampus in control group. Compared with control group, the model group significantly increased the number of apoptotic cells. Compared with model group, the number of apoptotic cells was significantly decreased in rat cortex and hippocampus (CA1, CA3, and DG) after treated with SPJ (10, 30, and 60 mg/kg). Western blotting results showed a significant age-related increase in the expression of IL-1β, ASC, NLRP3, NLRP1, Caspase-1, and IL-18, while SPJ concentration-dependently decreased the levels of IL-1β, ASC, NLRP3, NLRP1, Caspase-1, and IL-18 after six-month treatment. Conclusion In conclusion, saponins from P. japonicus has protective effects on the brain (cortex and hippocampus) of aging rats. The mechanism is likely to be that saponins from P. japonicus can reduce nerve inflammation by regulating NLRP1 and NLRP3 inflammasome pathway.
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WPRIM
Idioma:
Zh
Revista:
Zhongcaoyao
Año:
2017
Tipo del documento:
Article