Berberine activates Nrf2 nuclear translocation and protects against oxidative damage via a phosphatidylinositol 3-kinase/Akt-dependent mechanism in NSC34 motor neuron-like cells

Hsu, Ya Yun; Chen, Cheng Sheng; Wu, Sheng‐Nan; Jong, Yuh Jyh; Lo, Yi-Ching

doi:10.1016/j.ejps.2012.03.004

Cited by 130 publications

(79 citation statements)

References 48 publications

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“…Interestingly, increasing levels of reactive oxygen species (ROS) formation and subsequent oxidative stress have been shown to enhance aberrant alternative splicing in vitro and in vivo, with Wan et al observing that ROS causes crosslinking and inactivation of the SMN complex, a redox-assemblysome whose deficiency causes spinal muscular atrophy and is essential for the biogenesis of small nuclear ribonucleoproteins (snRNPs), major constituents of the spliceosome [91,92]. Reduction of oxidative stress and an increase in antioxidant enzyme levels are each associated with the upregulation of the Nrf2 antioxidant response pathway by the AMPK activators resveratrol, metformin, and berberine [93][94][95].…”

Section: Srsf1 Is Upregulated In Cancermentioning

confidence: 96%

Alteration of splice site selection in the LMNA gene and inhibition of progerin production via AMPK activation

Finley¹

2014

Medical Hypotheses

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Section: Srsf1 Is Upregulated In Cancermentioning

confidence: 96%

Alteration of splice site selection in the LMNA gene and inhibition of progerin production via AMPK activation

Finley¹

2014

Medical Hypotheses

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“…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). BBR has also been reported to induce nuclear translocation of the nuclear factor erythroid-2-related factor-2 (Nrf2), which activates the expression of antioxidant enzymes with a resultant reduction in oxidative stress (Hsu et al, 2012). Furthermore, BBR supplementation in rats increased the expression of sirtuin 1 (SIRT1), a deacetylase with antioxidant activity (Gomes et al, 2012).…”

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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“…Therefore, the mechanisms that have been described include different signaling pathways, among which are those where the transcription factors are sensitive to change due to redox state such as Nrf2, NFκB, AP-1, and HSF1. These transcription factors are known to simultaneously activate different cellular response to stress by triggering parallel response mechanisms, since most of them can regulate the expression of antioxidant enzymes and survival proteins (Mukherjee et al 2013;Hsu et al 2012;Jacobs and Marnett 2007;Zanotto-Filho et al 2009). …”

Section: Parallel Mechanisms During Hormetic Oxidative Responsementioning

confidence: 99%

New considerations on hormetic response against oxidative stress

Luna–López

González-Puertos

López‐Díazguerrero

et al. 2014

J. Cell Commun. Signal.

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In order to survive living organisms have developed multiple mechanisms to deal with tough environmental conditions. Hormesis is defined as a process in which exposure to a low dose of a chemical agent or environmental factor that is damaging at higher doses induces an adaptive beneficial effect on the cell or organism. In this paper, we examine several ideas that might be taken into consideration before using hormesis as a therapeutic tool to improve health and life span, and hopefully will open the discussion for new and interesting debates regard hormesis. The first one is to understand that the same stressor or inductor can activate different pathways in a parallel or dual response, which might lead to diverse outcomes. Another idea is related to the mechanisms involved in activating Nrf2, which might be different and have diverse hormetic effects.Last, we discuss mild oxidative stress in association to lowgrade chronic inflammation as a stimulating avenue to be explored and the unexpected effects proposed by the obesity paradox theory. All the previous might help to clarify the reasons why centenarians are able to reach the extreme limits of human life span, which could probably be related to the way they deal with homeostasis maintenance, providing an opportunity for hormesis to intervene significantly.

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Berberine activates Nrf2 nuclear translocation and protects against oxidative damage via a phosphatidylinositol 3-kinase/Akt-dependent mechanism in NSC34 motor neuron-like cells

Cited by 130 publications

References 48 publications

Alteration of splice site selection in the LMNA gene and inhibition of progerin production via AMPK activation

Alteration of splice site selection in the LMNA gene and inhibition of progerin production via AMPK activation

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

New considerations on hormetic response against oxidative stress

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