Cinnamon and its Metabolite Protect the Nigrostriatum in a Mouse Model of Parkinson’s Disease Via Astrocytic GDNF

Patel, Dhruv; Jana, Arundhati; Roy, Avik; Pahan, Kalipada

doi:10.1007/s11481-019-09855-0

Cited by 30 publications

(31 citation statements)

References 57 publications

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“…Recent in vitro data have shown that treatment of mouse and human astrocytes with sodium benzoate was associated with GDNF upregulation through recruitment of CREB to the promoter of the Gdnf gene, inducing its transcription. [ 19 ] This is in accordance with other studies showing that sodium benzoate activates CREB pathway in the brain by upregulating protein kinase A. [ 10,28 ]…”

Section: Effects Of Cinnamon and Its Metabolites In Pd: In Vitro Evidsupporting

confidence: 91%

Neuroprotective potential of cinnamon and its metabolites in Parkinson's disease: Mechanistic insights, limitations, and novel therapeutic opportunities

Angelopoulou

Paudel

Piperi

et al. 2021

J Biochem & Molecular Tox

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Parkinson's disease (PD) is the most common neurodegenerative movement disorder with obscure etiology and no disease‐modifying therapy to date. Hence, novel, safe, and low cost‐effective approaches employing medicinal plants are currently receiving increased attention. A growing body of evidence has revealed that cinnamon, being widely used as a spice of unique flavor and aroma, may exert neuroprotective effects in several neurodegenerative diseases, including PD. In vitro evidence has indicated that the essential oils of Cinnamomum species, mainly cinnamaldehyde and sodium benzoate may protect against oxidative stress‐induced cell death, reactive oxygen species generation, and autophagy dysregulation, thus acting in a potentially neuroprotective manner. In vivo evidence has demonstrated that oral administration of cinnamon powder and sodium benzoate may protect against dopaminergic cell death, striatal neurotransmitter dysregulation, and motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine mouse models of PD. The underlying mechanisms of its action include autophagy regulation, antioxidant effects, upregulation of Parkin, DJ‐1, glial cell line‐derived neurotrophic factor, as well as modulation of the TLR/NF‐κB pathway and inhibition of the excessive proinflammatory responses. In addition, in vitro and in vivo studies have shown that cinnamon extracts may affect the oligomerization process and aggregation of α‐synuclein. Herein, we discuss recent evidence on the novel therapeutic opportunities of this phytochemical against PD, indicating additional mechanistic aspects that should be explored, and potential obstacles/limitations that need to be overcome, for its inclusion in experimental PD therapeutics.

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Section: Effects Of Cinnamon and Its Metabolites In Pd: In Vitro Evidsupporting

confidence: 91%

Neuroprotective potential of cinnamon and its metabolites in Parkinson's disease: Mechanistic insights, limitations, and novel therapeutic opportunities

Angelopoulou

Paudel

Piperi

et al. 2021

J Biochem & Molecular Tox

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“…All data are mean ± SD. *P < 0.05; **P < 0.01 in vivo [41]. These results indicate that overactivated CREB is involved in regulating GDNF transcription in GBM cells.…”

Section: Discussionmentioning

confidence: 58%

Crosstalk between DNA methylation and histone acetylation triggers GDNF high transcription in glioblastoma cells

Zhang

Han

et al. 2020

Clin Epigenet

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Background: Glial cell line-derived neurotrophic factor (GDNF) is highly expressed in glioblastoma (GBM) and blocking its expression can inhibit the initiation and development of GBM. GDNF is a dual promoter gene, and the promoter II with two enhancers and two silencers plays a major role in transcription initiation. We had previously reported that histone hyperacetylation and DNA hypermethylation in GDNF promoter II region result in high transcription of GDNF in GBM cells, but the mechanism remains unclear. In this study, we investigated whether these modifications synergistically regulate high GDNF transcription in GBM. Results: Cyclic AMP response element binding protein (CREB) expression and phosphorylation at S133 were significantly increased in human GBM tissues and GBM cell lines (U251 and U343). In U251 GBM cells, high expressed CREB significantly enhanced GDNF transcription and promoter II activity. CREB regulated GDNF transcription via the cyclic AMP response elements (CREs) in enhancer II and silencer II of GDNF promoter II. However, the two CREs played opposite regulatory roles. Interestingly, hypermethylation of CRE in silencer II occurred in GBM tissues and cells which led to decreased and increased phosphorylated CREB (pCREB) binding to silencer II and enhancer II, respectively. Moreover, pCREB recruited CREB binding protein (CBP) with histone acetylase activity to the CRE of GDNF enhancer II, thereby increasing histone H3 acetylation and RNA polymerase II recruitment there and at the transcription start site (TSS), and promoted GDNF high transcription in U251 cells. The results indicated that high GDNF transcription was attributable to DNA hypermethylation in CRE of GDNF silencer II increasing pCREB binding to CRE in enhancer II, which enhanced CBP recruitment, histone H3 acetylation, and RNA polymerase II recruitment there and at the TSS. Conclusions: Our results demonstrate that pCREB-induced crosstalk between DNA methylation and histone acetylation at the GDNF promoter II enhanced GDNF high transcription, providing a new perspective for GBM treatment.

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“…The main functions of CS Presl include tonifying fire and helping yang, dispersing cold and relieving pain, warming blood vessels, improving yang deficiency, and treating vertigo. 122,123 The medicinal value of CS Presl is mainly reflected in antihypertensive, 124 anti-allergy, 125 antibacterial, 126 and anticancer 127 activities; it is used in the treatment of PD 128 and type 2 diabetes 129 and it improves cognitive dysfunction. 130 In addition, it enhances blood circulation and calms and relieves pain, and it has auxiliary therapeutic effects in depression.…”

Section: Rehmannia Glutinosa (Gaertn) DCmentioning

confidence: 99%

<p>Traditional Chinese Medicine Jiuwei Zhenxin Granules in Treating Depression: An Overview</p>

Wang

2020

NDT

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Depression is known as "Yu Zheng" in traditional Chinese medicine (TCM). Jiuwei Zhenxin granules (JZG) is a type of TCM. According to TCM theory, it nourishes the heart and spleen, tonifies Qi, and tranquilizes the spirit, and may also has effects in the treatment of depression. Here, we systematically reviewed recent basic and clinical experimental studies of JZG and depression, including studies of the pharmacological mechanisms, active ingredients, and clinical applications of JZG in depression treatment. This review will deepen our understanding of the pharmacological mechanisms, drug interactions, and clinical applications of TCM prescriptions and provide a basis for the development of new drugs in the treatment of depression.

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Cinnamon and its Metabolite Protect the Nigrostriatum in a Mouse Model of Parkinson’s Disease Via Astrocytic GDNF

Cited by 30 publications

References 57 publications

Neuroprotective potential of cinnamon and its metabolites in Parkinson's disease: Mechanistic insights, limitations, and novel therapeutic opportunities

Neuroprotective potential of cinnamon and its metabolites in Parkinson's disease: Mechanistic insights, limitations, and novel therapeutic opportunities

Crosstalk between DNA methylation and histone acetylation triggers GDNF high transcription in glioblastoma cells

<p>Traditional Chinese Medicine Jiuwei Zhenxin Granules in Treating Depression: An Overview</p>

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