Neuroprotective effect of crocin against rotenone-induced Parkinson's disease in rats: Interplay between PI3K/Akt/mTOR signaling pathway and enhanced expression of miRNA-7 and miRNA-221

Salama, Rania M.; Abdel‐Latif, Ghada A.; Abbas, Samah S.; Magdoub, Hekmat M. El; Schaalan, Mona F.

doi:10.1016/j.neuropharm.2019.107900

Cited by 92 publications

(52 citation statements)

References 56 publications

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“…Raghu et al (2009) reported, activation of Akt by G1-4A (a polysaccharide from Tc) [82]. In an attempt to unravel the anti-apoptotic action of Tc against ROTintoxication, our study revealed an increased expression of Akt1, also supported by Salama et al (2020) [83,84].…”

Section: Tiam1 (T Lymphoma Invasion and Metastasis 1) Is A Rac-speci mentioning

confidence: 57%

Unraveling the Neuroprotective Effect of Tinospora Cordifolia in Parkinsonian Mouse Model Through Proteomics Approach.

Birla

Keswani

Singh

et al. 2021

Preprint

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BackgroundStress-induced dopaminergic (DAergic) neuronal death in the midbrain region is the primary cause of Parkinson’s disease (PD). Approximately 2% of the global population aged above 65 years is affected with PD. Various factors are responsible for the death of DAergic neurons, among which mitochondrial dysfunction, oxidative stress, misfolded protein aggregation and neuroinflammation are the primary factors. From the discovery of L-dopa, multiple drugs were discovered to improve lifestyle of PD patients, but they failed due to their multiple side effects. Tinospora cordifolia (Tc), a medicinal herb has been used in traditional medicines to treat neurodegenerative diseases. In our previous study, the neuroprotective role of Tc against MPTP-intoxicated Parkinsonian mice was reported. Here, we further explore the neuroprotective molecular mechanisms of Tc in Rotenone (ROT) intoxicated mouse model through proteomics approach.MethodsMice were pretreated with Tc extract by oral administration, followed by ROT-intoxication (2mg/kg body wt. for 35 days, subcutaneous). Rotarod, catalepsy, footprint and pole tests were carried out at 35th day to observe the neuroprotective effects of Tc on motor impairment caused by ROT in PD mice. Protein from nigrostriatal region of the mid brain was isolated, and label free quantification (LFQ) was carried out to identify differentially expressed protein (DEPs) in control vs. PD and PD vs. treatment group. Bioinformatics analysis of DEPs was carried out to explore the molecular pathway, cellular location, molecular function of proteins.ResultsIn this study, we report 800 DEPs in control vs. PD and 133 in PD vs. Treatment group. In silico tools clearly demonstrate significant enrichment of biochemical and molecular pathways with DEPs which are known to be important for PD progression, including, mitochondrial gene expression, hypothetical network for drug addiction, PD pathways, TGF-β signaling, Alzheimer’s disease, Odorant GPCRs and chemokine signaling pathway.ConclusionThis study provides a novel insight for the disease progression in PD mouse. More importantly, it demonstrates that Tc exerts the therapeutic effects through the regulation of multiple pathways to protect DAergic neurons.

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Section: Tiam1 (T Lymphoma Invasion and Metastasis 1) Is A Rac-speci mentioning

confidence: 57%

Unraveling the Neuroprotective Effect of Tinospora Cordifolia in Parkinsonian Mouse Model Through Proteomics Approach.

Birla

Keswani

Singh

et al. 2021

Preprint

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“…Miravirsen is an antisense oligonucleotide that inhibits both DROSHA-and DICER -mediated processing of miR-122 precursors which enhance hepatitis C virus (HCV) genome transcription [45][46][47][48]. The role of miRNAs in various cellular processes has been established, including cell division and death, cellular development, proliferation, replicative senescence, intracellular signaling and aging [16,23,[49][50][51][52][53]. It is now clear that dysregulated expression of miRNAs can exert profound effects on cells function and, as a result, leads to various pathological and occasionally malignant outcomes [54][55][56][57].…”

Section: Clinical Applications Of Mirnasmentioning

confidence: 99%

“…It is now clear that dysregulated expression of miRNAs can exert profound effects on cells function and, as a result, leads to various pathological and occasionally malignant outcomes [54][55][56][57]. The involvement of miRNAs was showed in more than 70 different diseases such as cancer, viral infection, gastrointestinal malignancies, diabetes, immune-related diseases, and neurodegenerative disorders [51,53,[58][59][60][61][62][63][64]. In view of this, miRNAs are considered an interesting target for therapeutic intervention; to date, approximately 20 miRNA-and siRNA-based therapeutics are currently in the preclinical and/or in clinical trials [45,47].…”

Section: Clinical Applications Of Mirnasmentioning

confidence: 99%

Fecal microRNAs as Innovative Biomarkers of Intestinal Diseases and Effective Players in Host-Microbiome Interactions

Sarshar

Scribano

Ambrosi

et al. 2020

Cancers

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Over the past decade, short non-coding microRNAs (miRNAs), including circulating and fecal miRNAs have emerged as important modulators of various cellular processes by regulating the expression of target genes. Recent studies revealed the role of miRNAs as powerful biomarkers in disease diagnosis and for the development of innovative therapeutic applications in several human conditions, including intestinal diseases. In this review, we explored the literature and summarized the role of identified dysregulated fecal miRNAs in intestinal diseases, with particular focus on colorectal cancer (CRC) and celiac disease (CD). The aim of this review is to highlight one fascinating aspect of fecal miRNA function related to gut microbiota shaping and bacterial metabolism influencing. The role of miRNAs as “messenger” molecules for inter kingdom communications will be analyzed to highlight their role in the complex host-bacteria interactions. Moreover, whether fecal miRNAs could open up new perspectives to develop novel suitable biomarkers for disease detection and innovative therapeutic approaches to restore microbiota balance will be discussed.

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“…Crocin, a watersoluble carotenoid, is regarded as the quality marker for the quality control of saffron, which has been extensively used for the treatment of brain and cardiovascular diseases in traditional Tibetan medicine (Chinese Pharmacopoeia Commission, 2015, Figure 1). Crocin showed the effects of antiapoptosis, antioxidation, neuroprotection, and inhibition of mitochondrial dysfunction [16][17][18]. Our previous study found that crocin pretreatment improved learning and memory in rat under acute high-altitude hypoxia, and it could upregulate the level of SIRT1 and PGC-1α in the hippocampus [19].…”

Section: Introductionmentioning

confidence: 97%

Cognitive Protective Mechanism of Crocin Pretreatment in Rat Submitted to Acute High-Altitude Hypoxia Exposure

Zhang

Dang

et al. 2020

BioMed Research International

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Inadequate oxygen availability at high altitude leads to oxidative stress, resulting in hippocampal neurodegeneration and memory impairment. In our previous study, we found that the cognitive dysfunction occurred when male SD rat was rapidly exposed to 4200 m of high altitude for 3 days. And we also found that crocin showed a cognitive protective effect under hypoxia by regulating SIRT1/PGC-1α pathways in rat’s hippocampus. In this article, focused on factors related to SIRT1/PGC-1α pathways, we proposed to further elucidate crocin’s pharmacological mechanism. Adult male Sprague-Dawley rats were randomly divided into five groups: control group, hypoxia group (rats were rapidly transported to high altitude of 4200 m for 72 h), and crocins+hypoxia groups (pretreatment with crocin of 25, 50, and 100 mg/kg/d for 3 days). The learning and memory ability was tested by Morris water maze analysis. Hippocampal histopathological changes were observed by HE staining and Nissl staining. The expression of NRF1, TFAM, Bcl-2, Bax, and caspase-3 was detected by immunohistochemistry, RT-PCR, and western blotting test. The contents of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSHPx) were detected by the TBA, WST, and colorimetry method. Neuronal apoptosis was observed by TUNEL staining. After crocin pretreatment, the traveled distance was significantly reduced and the percentage of time in the target quadrant was significantly increased tested by Morris water maze. And neuronal damage in the hippocampus was also significantly ameliorated based on HE staining and Nissl staining. Furthermore, in hippocampus tissue, mitochondrial biosynthesis-related factors of NRF1, TFAM expression was increased; oxidative stress factors of SOD, GSH, and GSHPx expression level were increased, and MDA and glutathione disulfide (GSSG) level were decreased; antiapoptotic protein Bcl-2 expression was increased, and proapoptotic proteins Bax and caspase-3 expression were decreased, with a manner of crocin dose dependent. Therefore, the cognitive protective mechanism of crocin in rat under acute hypoxia was related to promoting mitochondrial biosynthesis, ameliorating oxidative stress injury, and decreasing neuronal apoptosis.

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Neuroprotective effect of crocin against rotenone-induced Parkinson's disease in rats: Interplay between PI3K/Akt/mTOR signaling pathway and enhanced expression of miRNA-7 and miRNA-221

Cited by 92 publications

References 56 publications

Unraveling the Neuroprotective Effect of Tinospora Cordifolia in Parkinsonian Mouse Model Through Proteomics Approach.

Unraveling the Neuroprotective Effect of Tinospora Cordifolia in Parkinsonian Mouse Model Through Proteomics Approach.

Fecal microRNAs as Innovative Biomarkers of Intestinal Diseases and Effective Players in Host-Microbiome Interactions

Cognitive Protective Mechanism of Crocin Pretreatment in Rat Submitted to Acute High-Altitude Hypoxia Exposure

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