Berberine improves endothelial function by reducing endothelial microparticles-mediated oxidative stress in humans

Cheng, Fei; Wang, Yan; Li, Jing; Su, Chen; Wu, Fang; Xia, Wenhao; Yang, Zhaohui; Yu, Bingqing; Qiu, Yan-Xia; Tao, Jun

doi:10.1016/j.ijcard.2012.03.090

Cited by 93 publications

(71 citation statements)

References 40 publications

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“…In the diabetic state, BBR treatment up-regulated mRNA expression of SOD and increased the contents of SOD, GSH, and GPx in rat liver (Zhou and Zhou, 2011). BBR decreased the expression level of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a major source of ROS production (Cheng et al, 2013). BBR treatment attenuated non-alcoholic fatty liver disease in rats through up-regulation of uncoupling protein 2 (UCP2) expression, a mitochondrial inner membrane protein that is negatively associated with ROS production and oxidative stress (Yang et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Modulatory effect of berberine on adipose tissue PPARγ, adipocytokines and oxidative stress in high fat diet/ streptozotocin-induced diabetic rats

2017

J App Pharma Sci

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The current study was designed to investigate the anti-hyperglycemic and antioxidant effects of berberine (BBR) in high fat diet/streptozotocin (HFD/STZ)-induced type 2 diabetic rats, focusing on the role of adipose tissue peroxisome proliferator activated receptor gamma (PPARγ), resistin and inflammatory cytokines. Type 2 diabetes was induced by feeding rats with HFD for 4 weeks followed by a single intraperitoneal injection of 35 mg/kg body weight STZ. Diabetic rats were supplemented with 50 and 100 mg/kg BBR orally for 4 weeks. HFD/STZ-induced diabetic rats showed a significant increase in serum glucose and fructoseamine, and significant decrease in body weight and serum insulin. Serum pro-inflammatory cytokines were significantly increased in serum of the diabetic rats. BBR significantly ameliorated body weight, and serum glucose, insulin and pro-inflammatory cytokines. In addition, diabetic rats exhibited a significant increase in liver lipid peroxidation and nitric oxide levels, and declined antioxidant defenses, an effect that was reversed following treatment with BBR. Adipose tissue PPARγ mRNA was significantly down-regulated while resistin mRNA was markedly up-regulated in diabetic rats. BBR treatment significantly ameliorated both PPARγ and resistin mRNA expression. In conclusion, BBR attenuates hyperglycemia and its associated oxidative stress and inflammation, possibly through potentiation of the antioxidant defenses and up-regulation of PPARγ expression.

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Section: Discussionmentioning

confidence: 99%

Modulatory effect of berberine on adipose tissue PPARγ, adipocytokines and oxidative stress in high fat diet/ streptozotocin-induced diabetic rats

2017

J App Pharma Sci

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“…These results are consistent with the literature. Several studies have shown that NOX4-based NADPH oxidase activity is apocynin sensitive (4,9,12,22,62,69,83,93). There is also an abundance of evidence that apocynin is effective for inhibiting NOX1 in a variety of tissues (11,12,17,45,85,90,93,95).…”

Section: We Hypothesized That Ang II Stimulates Omentioning

confidence: 99%

Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4

Massey

Hong

Garvin

2012

American Journal of Physiology-Cell Physiology

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Angiotensin II (ANG II) stimulates production of superoxide (O(2)(-)) by NADPH oxidase (NOX) in medullary thick ascending limbs (TALs). There are three isoforms of the catalytic subunit (NOX1, 2, and 4) known to be expressed in the kidney. We hypothesized that NOX2 mediates ANG II-induced O(2)(-) production by TALs. To test this, we measured NOX1, 2, and 4 mRNA and protein by RT-PCR and Western blot in TAL suspensions from rats and found three catalytic subunits expressed in the TAL. We measured O(2)(-) production using a lucigenin-based assay. To assess the contribution of NOX2, we measured ANG II-induced O(2)(-) production in wild-type and NOX2 knockout mice (KO). ANG II increased O(2)(-) production by 346 relative light units (RLU)/mg protein in the wild-type mice (n = 9; P < 0.0007 vs. control). In the knockout mice, ANG II increased O(2)(-) production by 290 RLU/mg protein (n = 9; P < 0.007 vs. control). This suggests that NOX2 does not contribute to ANG II-induced O(2)(-) production (P < 0.6 WT vs. KO). To test whether NOX4 mediates the effect of ANG II, we selectively decreased NOX4 expression in rats using an adenovirus that expresses NOX4 short hairpin (sh)RNA. Six to seven days after in vivo transduction of the kidney outer medulla, NOX4 mRNA was reduced by 77%, while NOX1 and NOX2 mRNA was unaffected. In control TALs, ANG II stimulated O(2)(-) production by 96%. In TALs transduced with NOX4 shRNA, ANG II-stimulated O(2)(-) production was not significantly different from the baseline. We concluded that NOX4 is the main catalytic isoform of NADPH oxidase that contributes to ANG II-stimulated O(2)(-) production by TALs.

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“…In vitro, berberine inhibits the secretion of NO, ET-1, TNFα, IL-1α, IL-6, IL-8, E-selectin and TXB2 from rat intestinal microvascular endothelial cells (RIMECs) in response to LPS stimulus [12,13]. In addition, berberine reduces circulating microparticles, inhibits apoptosis of leukocyte-mediated endothelium [14], activates peroxisome proliferator-activated receptor gamma (PPARγ) and suppresses oxidative stress [15,16], ameliorates vascular permeability and increases tight junction by the upregulation of claudins (e.g., claudin-5) [17]. In the present study we aimed to investigate whether berberine might protect GVB via the modulation of the Wnt/beta-catenin signaling pathway, which can be blocked by inhibitor ICG001 both in vivo and vitro experiments [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Berberine Exerts a Protective Effect on Gut-Vascular Barrier via the Modulation of the Wnt/Beta-Catenin Signaling Pathway During Sepsis

Yuan

Zuo

et al. 2018

Cell Physiol Biochem

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Background/Aims: The gut-vascular barrier (GVB) has recently been depicted to dampen the bacterial invasion of the bloodstream. The intestinal mucosa is a tissue rich in small vessels including capillaries. In this study, the protective effect of berberine on GVB in small bowel mucosa was investigated. Methods: The rat cecal ligation and puncture (CLP) sepsis model was employed to evaluate the effect of berberine on serum endotoxin level and intestinal vascular permeability to Evans blue in vivo. The rat intestinal microvascular endothelial cells (RIMECs) treated by lipopolysaccharide (LPS) were used to assess the effect of berberine on endothelial permeability to FITC-labeled dextran, transendothelial electrical resistance (TEER), and tight junction (TJ) and adherens junction (AJ) expression in vitro. Results: After 24-hr CLP operation the serum endotoxin concentration and gut vascular permeability were significantly increased, while berberine markedly reduced endotoxin level and vascular leakage. In vitro, LPS not only dramatically increased endothelial permeability of RIMECs to FITC-dextran, but also decreased TEER and inhibited claudin-12, beta-catenin and VE-cadherin expression. These effects of LPS were antagonized by berberine. In addition, our in vivo and vitro studies also confirmed that the effect of berberine on GVB could be partially abolished by ICG001. Conclusion: Berberine exerted a protective effect on GVB function in sepsis, which was strictly related to the modulation of the Wnt/beta-catenin signaling pathway.

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Berberine improves endothelial function by reducing endothelial microparticles-mediated oxidative stress in humans

Cited by 93 publications

References 40 publications

Modulatory effect of berberine on adipose tissue PPARγ, adipocytokines and oxidative stress in high fat diet/ streptozotocin-induced diabetic rats

Modulatory effect of berberine on adipose tissue PPARγ, adipocytokines and oxidative stress in high fat diet/ streptozotocin-induced diabetic rats

Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4

Berberine Exerts a Protective Effect on Gut-Vascular Barrier via the Modulation of the Wnt/Beta-Catenin Signaling Pathway During Sepsis

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