Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Dec;58(1):959-968.
doi: 10.1080/13880209.2020.1817102.

Polysaccharide of Taxus chinensis var. mairei Cheng et L.K.Fu attenuates neurotoxicity and cognitive dysfunction in mice with Alzheimer's disease

Senwei Zhang  1 , Lulu Li  2 , Jinting Hu  1 , Ping Ma  3 , Huimin Zhu  4
Affiliations

Polysaccharide of Taxus chinensis var. mairei Cheng et L.K.Fu attenuates neurotoxicity and cognitive dysfunction in mice with Alzheimer's disease

Senwei Zhang et al. Pharm Biol. 2020 Dec.

Abstract

Context: Polysaccharide of Taxus chinensis var. mairei Cheng et L.K.Fu (Taxaceae) (PTM) functions in anti-apoptosis and antioxidation, but its function on Alzheimer's disease (AD) remains unclear.

Objective: To investigate the effect of PTM on AD.

Materials and methods: C57BL/6J mice were randomly divided into three groups: control, d-galactose (d-gal), and d-gal + PTM. AD-like symptom was induced by d-gal for 6 weeks, followed with PTM (0.4 g/kg/d) for 14 days. PTM was added to BV2 cells stimulated with d-gal (1, 10, 20, 50, 100 and 500 μg/mL). Cell viability was evaluated by MTT assay. The expression of NRF2, SOD, cleaved caspase-3, Bax and Bcl-2 were detected with Western blot analysis. Cognitive function was evaluated by Morris water maze test.

Results: Decreased cleaved caspase-3 (1.30 ± 0.09) and Bax/Bcl2 ratio (1.32 ± 0.11) were observed in BV2 cells induced by d-gal + PTM (50 μg/mL). Increased MDA and ROS and decreased SOD were observed in d-gal group. However, decreased MDA (175 ± 9 ng/mL) and ROS level (188 ± 38 ng/mL) were observed after treated with PTM group (p < 0.05). In addition, the expression of NRF2 decreased in d-gal group (0.75 ± 0.09) but increased after treated with PTM (p < 0.05). Furthermore, decreased Aβ1-42 was observed and the cognitive function was improved after PTM intervention (p < 0.05).

Conclusions: This is the first report that PTM inhibited oxidative stress and apoptosis in AD. The result will further accelerate the applications of Taxus chinensis var. mairei and the treatment for AD.

Keywords: Oxidative stress; apoptosis; spatial learning ability.

PubMed Disclaimer

Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Polysaccharide of Taxus chinensis var. mairei (PTM) pre-treatment protected BV2 cells against d-gal-induced cell death.
Figure 2.
Figure 2.
Polysaccharide of Taxus chinensis var. mairei (PTM) decreased attenuated the d-gal induced apoptosis in BV2 cells.
Figure 3.
Figure 3.
Effects of polysaccharide of Taxus chinensis var. mairei (PTM) on oxidative stress in BV2 cells treated with d-gal.
Figure 4.
Figure 4.
Si-NRF2 abrogated effect of polysaccharide of Taxus chinensis var. mairei (PTM) on d-gal-treated cells.
Figure 5.
Figure 5.
Si-NRF2 diminished benefits of polysaccharide of Taxus chinensis var. mairei (PTM) on d-gal-treated cells.
Figure 6.
Figure 6.
Polysaccharide of Taxus chinensis var. mairei (PTM) improved histopathological changes and d-gal induced apoptosis in mice brain.
Figure 7.
Figure 7.
Polysaccharide of Taxus chinensis var. mairei (PTM) increased NRF2 expression and decreased oxidative stress.
Figure 8.
Figure 8.
Polysaccharide of Taxus chinensis var. mairei (PTM) attenuated d-gal induced recognition impairments in mice.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Barone S Jr, Das KP, Lassiter TL, White LD.. 2000. Vulnerable processes of nervous system development: a review of markers and methods. Neurotoxicol. 21:15–36. - PubMed
    1. Berlit P, Keyvani K, Kramer M, Weber R.. 2015. Cerebral amyloid angiopathy and dementia. Nervenarzt. 86(10):1248–1254. - PubMed
    1. Chandra SR. 2017. Alzheimer’s disease: an alternative approach. Indian J Med Res. 145(6):723–729. - PMC - PubMed
    1. Chang YJ, Linh NH, Shih YH, Yu HM, Li MS, Chen YR.. 2016. Alzheimer’s amyloid-β sequesters caspase-3 in vitro via its C-terminal tail. ACS Chem Neurosci. 7(8):1097–1106. - PubMed
    1. Cheignon C, Tomas M, Bonnefont-Rousselot D, Faller P, Hureau C, Collin F.. 2018. Oxidative stress and the amyloid beta peptide in Alzheimer’s disease. Redox Biol. 14:450–464. - PMC - PubMed

MeSH terms