ArticleExperimental and therapeutic medicine2019
Effect of PI3K/Akt/mTOR signaling pathway on JNK3 in Parkinsonian rats.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- JNK3 quantification in plasma: a novel biomarker for neuronal damage in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Improving Alzheimer's Disease and Parkinson's Disease in Rats with Nanoemulsion and Byproducts Prepared from Cinnamon Leaves.Pharmaceutics · 2025Article
- Article
- eEF1A2 siRNA Suppresses MPPTheScientificWorldJournal · 2023Article
- To re-examine the intersection of microglial activation and neuroinflammation in neurodegenerative diseases from the perspective of pyroptosis.Frontiers in aging neuroscience · 2023Review
- PI3K/AKT/mTOR signalling inhibitor chrysophanol ameliorates neurobehavioural and neurochemical defects in propionic acid-induced experimental model of autism in adult rats.Metabolic brain disease · 2022Article
- Neuroprotective Effect of Chrysophanol as a PI3K/AKT/mTOR Signaling Inhibitor in an Experimental Model of Autologous Blood-induced Intracerebral Hemorrhage.Current medical science · 2022Article
- Article
- Review
- Therapeutic Potential ofFrontiers in pharmacology · 2020Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effect of PI3K/Akt/mTOR signaling pathway on the expression of JNK3 in Parkinsonian rats was investigated. A total of 200 rats were used for Parkinson's disease (PD) modeling and 180 models were successfully established. Rats were randomly divided into four groups including A, B, C, and D, 45 in each group. Group A was control group and no inhibitor was given. Group B was given PI3K inhibitor LY294002. Group C was given rapamycin inhibitor rapamycin; and group D was given inhibitor LY294002 and inhibitor rapamycin. JNK3 mRNA expression was detected by RT-qPCR and expression of p-mTOR protein and JNK3 protein was detected by western blot analysis. Expression level of JNK3 mRNA and protein in groups C and D was significantly lower than that in group B (P<0.01). Expression level of JNK3 mRNA and protein in group D was significantly lower than that in group C (P<0.01). Relative expression level of p-mTOR protein in groups C and D was significantly lower than that in group B (P<0.01). Relative expression level of JNK3 protein in group D was significantly lower than that in group C (P<0.01). Pearson's correlation analysis showed that expression of JNK3 mRNA was positively correlated with the expression of JNK3 protein and Pearson's correlation coefficient was 0.98 (P<0.01). There was also a positive correlation between the expression of JNK3 mRNA and the expression of p-mTOR protein and Pearson's correlation coefficient was 0.95 (P<0.01). Expression of JNK3 protein was positively correlated with the expression of p-mTOR protein, and the Pearson's correlation coefficient was 0.93 (P<0.01). Inhibition of PI3K/Akt/mTOR signaling pathway is negatively correlated with the expression of JNK3. Inhibition of PI3K-Akt-mTOR signaling pathway leads to a decrease in the expression of JNK3, which protects dopaminergic neurons and improves PD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.