ArticleChinese journal of integrative medicine2017
Neuroprotective effects of Tongmai Yizhi Decoction () against Alzheimer's disease through attenuating cyclin-dependent kinase-5 expression.
Article in Chinese journal of integrative medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Disease-Modifying Activity of Huperzine A on Alzheimer's Disease: Evidence from Preclinical Studies on Rodent Models.International journal of molecular sciences · 2022Review
- A Synopsis of Multitarget Potential Therapeutic Effects of Huperzine A in Diverse Pathologies-Emphasis on Alzheimer's Disease Pathogenesis.Neurochemical research · 2022Review
- Selected Natural Products in Neuroprotective Strategies for Alzheimer's Disease-A Non-Systematic Review.International journal of molecular sciences · 2022Review
- Review
- Therapeutic Effects of Natural Drugs on Alzheimer's Disease.Frontiers in pharmacology · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
objectivesTo explore the protective effects of Tongmai Yizhi Decoction (, TYD), a Chinese herb complex prescription against the impairment of cognitive functions and memory loss in amyloid beta 1-40 (Aβ
methodsThe in vivo model was established by injecting Aβ
resultsAβ1-40 and IBO treatment induced longer escape latency of rats, compared with sham operation group from day 25 (P<0.01). However, TYD and huperzine A obviously shortened the escape latency from day 26 (P<0.01). Moreover, the effect of TYD was similar to huperzine A (P>0.05). Furthermore, HE staining also showed that TYD and huperzine A reversed the neuropathological changes in the hippocampus triggered by Aβ1-40 and IBO. TYD and huperzine A effectively reduced the expression levels of Cdk5 protein and gene located in rat hippocampus, compared with the AD model group (P<0.01).
conclusionTYD could be a promising neuroprotective agent for protecting neuron from AD injury through inhibiting Cdk5 expression.
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