Protective effects of carnosic acid against aging in a premature cellular senescence model and in a D-galactose induced mouse model
10.16438/j.0513-4870.2019-0826
- VernacularTitle:鼠尾草酸对H2O2诱导的早熟性细胞衰老和D-半乳糖诱导的衰老模型小鼠的保护作用
- Author:
Hui-li SU
1
;
Yi-zhong BAO
1
;
Jing ZHANG
1
;
Xiao-gang XU
1
;
Zhong-shan ZHANG
2
;
Xiao-qing WAN
1
;
Gen-xiang MAO
1
Author Information
1. Zhejiang Hospital, Hangzhou 310013, China
2. School of Life Sciences, Huzhou University, Huzhou 313000, China
- Publication Type:Research Article
- Keywords:
carnosic acid;
aging;
italic>D-galactose;
non-enzymatic glycosylation;
oxidative stress
- From:
Acta Pharmaceutica Sinica
2020;55(5):915-921
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed to investigate the effect and possible mechanism of carnosic acid (CA) on delaying aging. The effects of CA on senescence-related β-galactosidase (SA-β-Gal) activity and expressions of p53, p21 and p16 were evaluated by an oxidative challenge induced premature 2BS cell senescence model. Meanwhile, the animal experiment was approved by the Ethics Committee of Zhejiang Hospital. Male C57 BL/6J mice were injected with 100 mg·kg-1·d-1 D-galactose (D-gal) for 8 weeks to establish an aging model in vivo, and CA at 5 and 10 mg·kg-1·d-1 were given ig administration at the same time. Morris water maze test was used to test the spatial memory ability. Then the serum and tissue samples were collected for the detections of malondialdehyde (MDA), total superoxide dismutase (T-SOD), interleukin-6 (IL-6), tumor necrosis factor α (TNFα) and advanced glycation end products (AGEs) as well as the protein expression of p53, p21 and p16 in hippocampus of brain. The results showed that H2O2 induced increment of SA-β-Gal activity (95%) was prevented by CA treatment (35%) and the enhanced protein expressions of p53, p21 and p16 in H2O2 exposed 2BS cells were alleviated by CA treatment, suggesting a potent protective role of CA against premature senescence induced by oxidative challenge. For in vivo study, D-gal induced declined spatial memory ability was partly reversed by CA administration. Besides, the serum and cerebral levels of MDA, IL-6, TNFα and AGEs were attenuated by CA treatment when compared to those in model mice. And the protein expressions of p53, p21 and p16 in mice hippocampus were suppressed by CA in D-gal treated mice. Taken together, our results showed that CA protects premature senescence induced by oxidative stress and D-gal, which is related to its antioxidative, antiinflammatory roles and inhibition on non-enzymatic glycosylation.
