Increased Bioavailable Berberine Protects Against Myocardial Ischemia Reperfusion Injury Through Attenuation of NFκB and JNK Signaling Pathways

Yu, Yang; Zhang, Ming; Hu, Yali; Zhao, Yali; Teng, Fei; Lv, Xiaoyan; Li, Ji; Zhang, Ying; Hatch, Grant M.; Chen, Li

doi:10.1536/ihj.17-458

Cited by 34 publications

(20 citation statements)

References 33 publications

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“…Berberine (1, Figure 1) is one of the best characterized natural compounds with diverse pharmacological effects, including anticancer [5][6][7], anti-inflammatory [8,9], cardioprotective [10,11] and enhancement of memory function [12][13][14] effects. Its antidiabetic [15][16][17], antiobesity and anti-hyperlipidaemic [16,18] effects have also been well established.…”

Section: Introductionmentioning

confidence: 99%

The Quest to Enhance the Efficacy of Berberine for Type-2 Diabetes and Associated Diseases: Physicochemical Modification Approaches

Habtemariam

2020

Biomedicines

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Berberine is a quaternary isoquinoline alkaloid that has been isolated from numerous plants which are still in use today as medicine and herbal supplements. The great deal of enthusiasm for intense research on berberine to date is based on its diverse pharmacological effects via action on multiple biological targets. Its poor bioavailability resulting from low intestinal absorption coupled with its efflux by the action of P-glycoprotein is, however, the major limitation. In this communication, the chemical approach of improving berberine’s bioavailability and pharmacological efficacy is scrutinised with specific reference to type-2 diabetes and associated diseases such as hyperlipidaemia and obesity. The application of modern delivery systems, research from combination studies to preparation of berberine structural hybrids with known biologically active compounds (antidiabetic, antihyperlipidaemic and antioxidant), as well as synthesis approaches of berberine derivative are presented. Improvement of bioavailability and efficacy through in vitro and ex vivo transport studies, as well as animal models of bioavailability/efficacy in lipid metabolism and diabetes targets are discussed.

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Section: Introductionmentioning

confidence: 99%

The Quest to Enhance the Efficacy of Berberine for Type-2 Diabetes and Associated Diseases: Physicochemical Modification Approaches

Habtemariam

2020

Biomedicines

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“…The genome-wide investigations of genetic variants, epigenetic modifications, and gene expression profiles optimize the search for novel diagnostic or therapeutic targets for IR injury in the postgenomic era 4 . MicroRNAs (miRNAs) are a class of small endogenous noncoding RNAs with [19][20][21][22][23][24][25] nucleotides in length, which modulate gene expression at the post-transcriptional level 5,6 . A systematic comparison of IR injury-induced miRNA expression changes in rats identifies several potential cardioprotective miRNA targets (protectomiRs), including Rno-miR-125b*, -139-3p, -320, -532-3p, and -188 7 .…”

Section: Introductionmentioning

confidence: 99%

Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1

Chen

Zhang

et al. 2020

Preprint

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Background: This study aimed to investigate the regulatory effect of rno-microRNA-30c-5p (rno-miR-30c-5p) on myocardial ischemia reperfusion (IR) injury in rats and the underlying molecular mechanisms.Methods: A rat model of myocardial IR injury was established. The infarct size was detected by 2,3,5-triphenyltetrazolium chloride staining. The pathologic changes of myocardial tissues were detected by hematoxylin-eosin staining. The apoptosis of myocardial cells was measured by TUNEL staining and flow cytometry. The mRNA expression of rno-miR-30c-5p and Sirtuin 1 (SIRT1) was detected by quantitative real-time PCR. The levels of IL-1β, IL-6 and TNF-α were detected by enzyme linked immunosorbent assay. The protein expression of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 was detected by Western blot. The interaction between rno-miR-30c-5p and SIRT1 was predicted by TargetScan, and further identified by dual luciferase reporter gene and RNA immunoprecipitation assay.Results: The myocardial IR injury model was successfully established in rats. IR induced the myocardial injury in rats and increased the expression of rno-miR-30c-5p. Overexpression of rno-miR-30c-5p enhanced the inflammation, promoted the apoptosis, and activated NF-κB pathway in IR myocardial cells. SIRT1 was the target gene of rno-miR-30c-5p. Silencing of SIRT1 reversed the effects of rno-miR-30c-5p inhibitor on the apoptosis and NF-κB pathway in IR myocardial cells.Conclusions: Rno-miR-30c-5p promoted the myocardial IR injury in rats through activating NF-κB pathway and down-regulating SIRT1.

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“…Myocardial infarction is one of the most common cause of death worldwide 15 . UP to now, more and more researches have been devoted to exploring new therapeutic targets of myocardial infarction, but the effect is not so ideal.…”

Section: Discussionmentioning

confidence: 99%

microRNA-30c promotes myocardial ischemia reperfusion injury by activating SIRT1 mediating NF-κB pathway

Chen

Xue

Zhang

et al. 2019

Preprint

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Background This study aimed to investigate the effect of miR-30c on myocardial ischemia reperfusion (IR) injury and its underlying molecular mechanisms.Methods In our study, rat myocardial IR injury model was established and hemodynamic examination was performed. Moreover, the myocardial infarct size was detected by TTC staining. The pathologic change of myocardial tissues was measured by HE staining. The myocardial cell apoptosis was measured by TUNEL staining and flow cytometry. The expression of miR-30c and Sirtuin 1 (SIRT1) was detected by qRT-PCR. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA. The expressions of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 were detected by western blot. The luciferase activity was measured by dual luciferase reporter gene assay. Interaction between miR-30c and SIRT1 were analyzed by RNA immunoprecipitation assay.Results Our results showed that rat myocardial IR injury model was successfully established and IR injury induced myocardial injury in rats. miR-30c increased the levels of IL-1β, IL-6 and TNF-α and myocardial cell apoptosis by activating NF-κB pathway. In addition, we also confirmed that SIRT1 was the target gene of miR-30c. SIRT1 could reverse the effect of miR-30c on the process of inflammation and apoptosis, as well as the activation of NF-κB pathway in myocardial cells.Conclusions Our study demonstrated that miR-30c could promote myocardial ischemia reperfusion injury through activating SIRT1 mediating NF-κB pathway.

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Increased Bioavailable Berberine Protects Against Myocardial Ischemia Reperfusion Injury Through Attenuation of NFκB and JNK Signaling Pathways

Cited by 34 publications

References 33 publications

The Quest to Enhance the Efficacy of Berberine for Type-2 Diabetes and Associated Diseases: Physicochemical Modification Approaches

The Quest to Enhance the Efficacy of Berberine for Type-2 Diabetes and Associated Diseases: Physicochemical Modification Approaches

Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1

microRNA-30c promotes myocardial ischemia reperfusion injury by activating SIRT1 mediating NF-κB pathway

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