Berberine confers neuroprotection in coping with focal cerebral ischemia by targeting inflammatory cytokines

Maleki, Solmaz Nasseri; Aboutaleb, Nahid; Souri, Faramarz

doi:10.1016/j.jchemneu.2017.04.008

Cited by 64 publications

(38 citation statements)

References 42 publications

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“…In their research, BBR has no effect on Akt or ERK 1/2 phosphorylation but reduces TLR4/MyD88/NF‐κB signaling. Through regulation of proinflammatory cytokines and anti‐inflammatory cytokines, BBR appeared to cope with focal cerebral ischemia and scopolamine‐induced neuronal impairment to exert its neuroprotection function (B. Lee, Sur, Shim, Lee, & Hahm, ; Maleki, Aboutaleb, & Souri, ). In addition to reduction of proinflammatory cytokines (TNFα, IL‐1β, and IL‐6) expression, BBR down‐regulates LPS‐ or IFN‐γ‐induced iNOS, NO, and COX‐2 in BV‐2 microglia cells through AMP‐activated protein kinase (AMPK) activation, which monitors the AMP/ATP ratio (D. Y. Lu et al, ).…”

Section: Inflammationmentioning

confidence: 99%

Berberine: Pathways to protect neurons

Lin

Zhang

2018

Phytotherapy Research

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Berberine, an isoquinoline alkaloid, is demonstrated to have a variety of pharmacologic effects. Widely used as nonprescription drug for diarrhea, berberine has also broadened its applications in therapies of cardiovascular diseases, diabetes mellitus, tumor, and so forth. However, researches about berberine's protective effects on nervous system are still so insufficient that clinical uses cannot popularize and underlying molecules mechanisms are confused and incomplete. Well-known pathways such as Pl3K/Akt/Bcl-2 pathway, Nrf2/HO-1 pathway, and MAPK signaling pathway help berberine to protect neurons through antiapoptotic, antioxidative, and anti-inflammatory activities. New hypotheses have been raised consistently to explore more possible ways of berberine preventing nerves from injuries as attention on its neuroprotective properties is increasing. Therefore, this review is trying to analyze these mechanisms, which actually play roles in neuronal disease models such as brain ischemia, Alzheimer's disease, and experimental autoimmune encephalomyelitis. Much more understanding about how berberine mediates these pathways provides novel insights into the clinical treatment of neurological disorders.

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Section: Inflammationmentioning

confidence: 99%

Berberine: Pathways to protect neurons

Lin

Zhang

2018

Phytotherapy Research

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“…In addition, it has been reported that a severer aspect of neuronal loss/death in the hippocampus is shown following 15 min of TFI than that in 5 min TFI in gerbils [ 2 ]. Furthermore, a rat model of focal brain ischemia induced by MCAO for over 1 h develops infarct lesion (necrotic tissue) which is easily visualized by 2, 3, 5-triphenyltetrazolium chloride (TTC) assay, but infarction does not occur in the brain induced by TFI for 5–15 min in gerbils when the TTC assay is applied, in which selective neuronal death only occurs [ 1 , 15 , 30 , 31 , 32 , 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that pro-inflammatory cytokines exacerbate and advance deleterious inflammatory processes, but anti-inflammatory cytokines suppress the expressions of pro-inflammatory cytokines and bring advantageous inflammatory processes in ischemic brains [ 10 , 52 ]. In this regard, many studies have reported that increases in anti-inflammatory cytokine expressions present neuroprotective effects following ischemia-reperfusion injuries [ 10 , 32 , 50 , 53 ]. In our current study, pro-inflammatory cytokines (TNF-α and IL-2) were increased in the CA1 pyramidal cells following TFI; however, pretreated 30 mg/kg CGA inhibited these increases and elevated the expression levels of anti-inflammatory cytokines (IL-4 and IL-13).…”

Section: Discussionmentioning

confidence: 99%

Experimental Pretreatment with Chlorogenic Acid Prevents Transient Ischemia-Induced Cognitive Decline and Neuronal Damage in the Hippocampus through Anti-Oxidative and Anti-Inflammatory Effects

et al. 2020

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Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is among the phenolic acid compounds which can be naturally found in green coffee extract and tea. CGA has been studied since it displays significant pharmacological properties. The aim of this study was to investigate the effects of CGA on cognitive function and neuroprotection including its mechanisms in the hippocampus following transient forebrain ischemia in gerbils. Memory and learning following the ischemia was investigated by eight-arm radial maze and passive avoidance tests. Neuroprotection was examined by immunohistochemistry for neuronal nuclei-specific protein and Fluoro-Jade B histofluorescence staining. For mechanisms of the neuroprotection, alterations in copper, zinc-superoxide dismutase (SOD1), SOD2 as antioxidant enzymes, dihydroethidium and 4-hydroxy-2-nonenal as indicators for oxidative stress, and anti-inflammatory cytokines (interleukin (IL)-4 and IL-13) and pro-inflammatory cytokines (tumor necrosis factor α (TNF-α) and IL-2) were examined by Western blotting and/or immunohistochemistry. As a result, pretreatment with 30 mg/kg CGA attenuated cognitive impairment and displayed a neuroprotective effect against transient forebrain ischemia (TFI). In Western blotting, the expression levels of SOD2 and IL-4 were increased due to pretreatment with CGA and, furthermore, 4-HNE production and IL-4 expressions were inhibited by CGA pretreatment. Additionally, pretreated CGA enhanced antioxidant enzymes and anti-inflammatory cytokines and, in contrast, attenuated oxidative stress and pro-inflammatory cytokine expression. Based on these results, we suggest that CGA can be a useful neuroprotective material against ischemia-reperfusion injury due to its antioxidant and anti-inflammatory efficacies.

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“…It has been shown that berberine when administered at nanomolar concentration it promotes cell survival and reduces oxidative stress by downregulating various factors such as cytochrome c, Bax and caspase. In the case of ischemic stroke, it has been observed that administration of berberine can protect by inhibiting potassium currents [ 60 ].…”

Section: Overview Of Phytochemicalsmentioning

confidence: 99%

Neuroprotective Role of Phytochemicals

et al. 2018

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Neurodegenerative diseases are normally distinguished as disorders with loss of neurons. Various compounds are being tested to treat neurodegenerative diseases (NDs) but they possess solitary symptomatic advantages with numerous side effects. Accumulative studies have been conducted to validate the benefit of phytochemicals to treat neurodegenerative diseases including Alzheimer’s disease (AD) and Parkinson’s disease (PD). In this present review we explored the potential efficacy of phytochemicals such as epigallocatechin-3-galate, berberin, curcumin, resveratrol, quercetin and limonoids against the most common NDs, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). The beneficial potentials of these phytochemicals have been demonstrated by evidence-based but more extensive investigation needs to be conducted for reducing the progression of AD and PD.

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Berberine confers neuroprotection in coping with focal cerebral ischemia by targeting inflammatory cytokines

Cited by 64 publications

References 42 publications

Berberine: Pathways to protect neurons

Berberine: Pathways to protect neurons

Experimental Pretreatment with Chlorogenic Acid Prevents Transient Ischemia-Induced Cognitive Decline and Neuronal Damage in the Hippocampus through Anti-Oxidative and Anti-Inflammatory Effects

Neuroprotective Role of Phytochemicals

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