Chlorogenic acid alleviates neurobehavioral disorders and brain damage in focal ischemia animal models

Shah, Murad-Ali; Kang, Ju-Bin; Park, Dong-Ju; Kim, Myeong-Ok; Koh, Phil-Ok

doi:10.1016/j.neulet.2021.136085

Cited by 32 publications

(18 citation statements)

References 40 publications

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Section: Methodsmentioning

confidence: 99%

“…Rats in the IR ± CGA group were administered twice at doses of 30 mg/kg of CGA (ip) 30,31 at 10 min before ischemia and 10 min before the beginning of reperfusion. The dose and the injection time of CGA were applied based on the previous studies 30–32 . Accordingly, Lee et al reported that administration of CGA at 3, 10, and 30 mg/kg ip could reduce brain infarct volume in a dose dependently manner, while only CGA at 30 mg/kg had significant neuroprotective effect 30 .…”

Section: Methodsmentioning

confidence: 99%

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miR‐23b/TAB3/NF‐κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia–reperfusion in rats: The protective effect of chlorogenic acid

et al. 2022

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Apoptosis is the main pathological aspect of neuronal injury after cerebral ischemia–reperfusion (I/R) injury. However the detailed molecular mediators are still under debate. The aim of this study is to explore the effect of cerebral I/R on miR‐23a/TGF‐β‐activated kinase 1 binding protein 3 (TAB3)/nuclear factor kappa B (NF‐κB)/p53 axis in rat hippocampus alone and in combination with chlorogenic acid (CGA). Common carotid artery occlusion (CCAO) was performed by nylon monofilament for 20 min to establish a model of ischemic brain injury. CGA (30 mg/kg) was administered intraperitoneally (ip), 10 min prior to ischemia and 10 min before reperfusion. Examination of hippocampus neurons by terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling staining showed that the number of apoptotic neurons was elevated at 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of p53 with a concomitant upregulation of cleaved‐caspase3/phosphorelated‐caspase3 ratio and cytochrome c level. Further miR‐23b gene expression was significantly downregulated after 24 h of reperfusion. Also, we observed increased TAB3 and NF‐κB protein expressions after 24 h following CCAO. Treatment with CGA significantly reduced the apoptotic damage and also reversed miR‐23b gene expression, TAB3 and NF‐κB protein expressions in hippocampus neurons in I/R rats. In conclusion our data suggest that miR‐23b/TAB3/NF‐κB/p53 axis could play a regulatory role in hippocampus cell death, which provide a new target for novel therapeutic interventions during transit ischemic stroke. It also demonstrated that CGA could reverse these molecular alterations indicating an effective component against hippocampus apoptotic insult following acute I/R injury.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

miR‐23b/TAB3/NF‐κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia–reperfusion in rats: The protective effect of chlorogenic acid

et al. 2022

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“…25–27 Additionally, recent research reported that dietary CGA could reverse cognitive impairment in Alzheimer's disease (AD) model mice 28,29 and alleviate neurobehavioral disorders in ischemia animal models. 30 However, the protective effects of CGA on TMT-induced neurobehavioral dysfunction have not been studied yet.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of chlorogenic acid on trimethyltin chloride-induced neurobehavioral dysfunctions in mice relying on the gut microbiota

et al. 2022

Food Funct.

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“…CA reduces apoptosis mediated by the miR-23b/TAB3/NF-κB pathway and decreases the release of inflammatory factors, thus acting as an anti-neuroinflammatory and anti-apoptotic agent [198]. Another study demonstrated that CA also regulates the expression of the apoptosis-related proteins caspase-3, caspase-7, and PARP and protects neurons from cerebral ischemia [197]. CA can downregulate intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) levels and upregulate targets such as erythropoietin (EPO), hypoxiainducible factor 1α (HIF-1α), and NGF levels in brain tissue, which reduces neuronal death and promotes neuronal regeneration [196].…”

Section: Cinnamic Acid Derivativesmentioning

confidence: 99%

Polyphenols for the Treatment of Ischemic Stroke: New Applications and Insights

et al. 2022

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Ischemic stroke (IS) is a leading cause of death and disability worldwide. Currently, the main therapeutic strategy involves the use of intravenous thrombolysis to restore cerebral blood flow to prevent the transition of the penumbra to the infarct core. However, due to various limitations and complications, including the narrow time window in which this approach is effective, less than 10% of patients benefit from such therapy. Thus, there is an urgent need for alternative therapeutic strategies, with neuroprotection against the ischemic cascade response after IS being one of the most promising options. In the past few decades, polyphenolic compounds have shown great potential in animal models of IS because of their high biocompatibility and ability to target multiple ischemic cascade signaling pathways, although low bioavailability is an issue that limits the applications of several polyphenols. Here, we review the pathophysiological changes following cerebral ischemia and summarize the research progress regarding the applications of polyphenolic compounds in the treatment of IS over the past 5 years. Furthermore, we discuss several potential strategies for improving the bioavailability of polyphenolic compounds as well as some essential issues that remain to be addressed for the translation of the related therapies to the clinic.

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Chlorogenic acid alleviates neurobehavioral disorders and brain damage in focal ischemia animal models

Cited by 32 publications

References 40 publications

miR‐23b/TAB3/NF‐κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia–reperfusion in rats: The protective effect of chlorogenic acid

miR‐23b/TAB3/NF‐κB/p53 axis is involved in hippocampus injury induced by cerebral ischemia–reperfusion in rats: The protective effect of chlorogenic acid

Protective effects of chlorogenic acid on trimethyltin chloride-induced neurobehavioral dysfunctions in mice relying on the gut microbiota

Polyphenols for the Treatment of Ischemic Stroke: New Applications and Insights

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