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Integrating network pharmacology, transcriptomics to reveal neuroprotective of curcumin activate PI3K / AKT pathway in Parkinson’s disease

ABSTRACT: Integrating network pharmacology, transcriptomics to reveal neuroprotective of curcumin activate PI3K / AKT pathway in Parkinson’s disease

PROVIDER: PRJNA1020412 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26156087_1.fastq.gz	Fastqsanger.gz
	SRR26156087_2.fastq.gz	Fastqsanger.gz
	SRR26156088_1.fastq.gz	Fastqsanger.gz
	SRR26156088_2.fastq.gz	Fastqsanger.gz
	SRR26156089_1.fastq.gz	Fastqsanger.gz

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Integrating network pharmacology, transcriptomics to reveal neuroprotective of curcumin activate PI3K / AKT pathway in Parkinson’s disease

Project description:Background: Parkinson’s disease (PD), a severe threat in aging society, is a significant cause of disable. Curcumin, a polyphenol with hydrophobic properties, has been proved to against Parkinson. Our previous study provides an initial understanding of the neuroprotective mechanisms of curcumin in treating Parkinson’s disease. However, further exploration in this area is needed. The present study was designed to investigate the potential mechanism of curcumin for treating PD. Methods: The therapeutic efficacy of curcumin was evaluated using behavioral tests, immunofluorescence of tyrosine hydroxylase (TH). Network pharmacology and transcriptomics predicted the active pathway and bioprocess of curcumin in PD. Activation of the PI3K / AKT signaling pathway was confirmed by quantitative real-time PCR and immunofluorescence. Result: Curcumin restored the dyskinesia and dopaminergic neurons damage of MPTP-induced mice. The results of network pharmacology and transcriptomics showed that curcumin against Parkinson's disease by regulating inflammation, oxidative stress, and aging. The mechanisms of these were associated with activation of PI3K / AKT pathway. Conclusion: In conclusion, the mechanism of curcumin against PD was revealed by our study which lays a foundation for the application of curcumin in treating.

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MC1R Basis of Melanoma - Parkinson’s Link and Neuroprotective Potential of MC1R

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Transcriptomics profiling of ccc_R08 for mechanism-of-action investigation with forward pharmacology

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Expression data from hippocampus and cortex of 6- and 12-week curcumin-treated 15-month-old rats

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_hMeDIP_Seq]

Project description:Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_hMeDIP_Seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2i_Bisulfite_Padlock_seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_TET2_Bisulfite_Padlock_Seq]

Project description:Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [PD_TET2_Bisulfite_Padlock_Seq]

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Epigenomic analysis of Parkinson’s disease neurons identifies TET2 loss as neuroprotective [TET2_LPS_RNA_Seq]

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Expression data from hippocampus and cortex of 6- and 12-week curcumin-treated 15-month-old rats

Project description:Curcumin has been demonstrated to have many neuroprotective properties, including improvement of cognition in humans and neurogenesis in animals, yet the mechanism of such effects remains unclear. Here, we assessed behavioural performance and hippocampal cell proliferation in aged rats after 6- and 12-week curcumin-fortified diets. Curcumin enhanced non-spatial and spatial memory, as well as dentate gyrate cell proliferation as compared to control diet rats. We also investigated underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via microarray analysis of cortical and hippocampal mRNA transcription. We used microarrays to investigate the effects of short-term (6-week) and long-term (12-week) curcumin-supplemented diet on gene expression of hippocampus and cortex in aged rats. The hippocampus and cortex of every three rats from one group were pooled together, respectively and used for RNA extraction and hybridization on Affymetrix microarrays. To ensure the reliability of the data, we conducted hybridization experiments in duplicate microarrays from each RNA sample. The tissues examined by microarray are as follows: the hippocampus and cortex of 6-week curcumin-treated 15-month-old rats, the hippocampus and cortex of 6-week no curcumin-treated 15-month-old rats (control rats), the hippocampus and cortex of 12-week curcumin-treated 15-month-old rats, the hippocampus and cortex of 12-week no curcumin-treated 15-month-old rats (control rats).

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Project description:Alpha-synuclein (α-syn) aggregation and immune activation represent hallmark pathological events in Parkinson’s disease (PD). The PD-associated immune response encompasses both brain and peripheral immune cells, although little is known about the immune proteins relevant for such response. We propose that the upregulation of CD163 observed in blood monocytes and in the responsive microglia in the PD patients is a protective mechanism in the disease. To investigate this, we used the PD model based on intrastriatal injections of murine α-syn pre-formed fibrils (PFF) in CD163 knockout (KO) mice and wild-type littermates. CD163KO females revealed an impaired and differential early immune response to α-syn pathology as revealed by immunohistochemical and transcriptomic analysis. After 6 months, CD163KO females showed an exacerbated immune response and α-syn pathology, which ultimately led to a dopaminergic neurodegeneration of greater magnitude. These findings support a novel, sex-dimorphic neuroprotective role for CD163 during α-syn-induced neurodegeneration.

2023-12-14 | GSE243536 | GEO

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