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Review
. 2017 May;20(5):557-568.
doi: 10.22038/IJBMS.2017.8682.

A review of the effects of Berberis vulgaris and its major component, berberine, in metabolic syndrome

Affiliations
Review

A review of the effects of Berberis vulgaris and its major component, berberine, in metabolic syndrome

Jamshid Tabeshpour et al. Iran J Basic Med Sci. 2017 May.

Abstract

Metabolic syndrome (MetS), characterized by a cluster of metabolic abnormalities including hypertension, obesity, type 2 diabetes mellitus (T2DM) and dyslipidemia, is a well-known cardiovascular risk factor (CVRF). Cardiovascular disease (CVD) represents a massive healthcare burden worldwide. In recent years, with regard to the adverse effects of synthetic drugs, increasing attention has been paid by researchers to herbal medicines for a variety of disorders such as CVD. A large body of literature supports different pharmacological actions of Berberis vulgaris (B. vulgaris) and its active component, berberine (BBR), such as antidiabetic, antiobesity, hypotensive and hypolipidemic properties that could be interesting in the management of MetS associated with high CVD risk. Numerous preclinical in vitro and in vivo studies support all these effects. In this review, we evaluated the most related original articles to discover the role of B. vulgaris on various constituents of MetS and CVRF comprising dyslipidemia, obesity, high blood pressure and high blood glucose. This review suggests a potential role of B. vulgaris and BBR in the managing of MetS; nevertheless more investigations, especially reliable clinical trials, need to be accomplished to evaluate their effectiveness.

Keywords: Berberine; Berberis vulgaris; Cardiovascular disease; Diabetes; Dyslipidemia; Hypertension; Metabolic syndrome.

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Figures

Figure 1
Figure 1
Berberis vulguris plant: showing leaves, flowers and fruits
Figure 2
Figure 2
Therapeutic effects of Berberis vulgaris and berberine on metabolic syndrome
Figure 3
Figure 3
Main mechanisms of berberine on glucose metabolism MAPK= mitogen-activated protein kinase; ERK= extracellular signal-regulated kinase; JNK= c-jun N-terminal kinase; STAT3= signal transducer and activator of transcription3; Th= T helper cells; PKC= protein kinase C; InsR= insulin receptor; IR= insulin resistance; MDA= malondialdehyde; SOD= superoxide dismutase; CAT= catalase; GSH= glutathione; G6Pase= glucose 6-phosphatase; AMPK= adenosine monophosphate-activated protein kinase; GLUT4= glucose transporter 4; PPARα= peroxisome proliferator-activated receptor α; UCP2= uncoupling protein 2; HNF4α= hepatic nuclear factor 4α; C/EBP= CCAAT enhancer-binding protein; PGC1α= PPARγ coactivator 1α; GLP-1= glucagon-like peptide-1; AC= adenylyl cyclase; cAMP= cyclic adenosine monophosphate; ATP= adenosine triphosphate; RBP4= retinol binding protein4; IL-6= interleukin 6; TNF-α= tumor necrosis factor; iNOS= inducible nitric oxide synthase; COX-2= cyclooxygenase-2; FtsZ= filamenting temperature-sensitive mutant Z; ROR= retinoic acid-related orphan receptors

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