Berberine protects against ischemia-reperfusion injury: A review of evidence from animal models and clinical studies

Liu, Dai-Qiang; Chen, Shuping; Sun, Jia; Wang, Xiaomei; Chen, Nan; Zhou, Ya‐Qun; Tian, Yuan; Ye, Dawei

doi:10.1016/j.phrs.2019.104385

Cited by 66 publications

(36 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, mitochondria-targeted agents, such as rotenone and metformin, also exhibit protective effects on cellular survival and extending lifespan at a low concentration via ROS-mediated mitohormetic signaling pathways (Yuyun et al 2012;De Haes et al 2014). This implied that mitochondria-targeted agents may produce a beneficial effect in aging-relative diseases via mitohormesis (Marcheggiani et al 2019;Bouitbir et al 2012;Liu et al 2019). Fig.…”

Section: Resultsmentioning

confidence: 99%

“…When the strength of stressors exceeded the adaptive capacity of cells, it could cause mitochondriamediated cell death (Valera-Alberni and Canto 2018; Lan et al 2019). In toxicology, this biphasic dose response, called as "hormesis," was observed in many natural active ingredients from traditional Chinese medicine (Wang et al 2018;Liu et al 2019). This phenomenon indicated that conventional "toxic" drugs may have beneficial effects on cells.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The mitohormetic response as part of the cytoprotection mechanism of berberine

Zhu

Wei

Yang

et al. 2020

Mol Med

View full text Add to dashboard Cite

It was well-known that Berberine, a major bioactive compound extracted from natural plants Coptis chinensis, has anti-diabetic effects for decades in china. Other types of pharmacological activities, such as anti-inflammatory, antimicrobial, hypolipidemic, and anti-cancer effects, have also been examined. At cellular level, these pharmacological activities were mostly an inhibitory effect. However, the cytoprotective effect of berberine was also observed in various types of cells, such as neurons, endothelial cells, fibroblasts, and β-cells. The paradoxical result may be closely associated with characteristics and distribution of berberine within cells, and they can be explained mechanically by mitohormesis, one particular form of hormesis. Here, we reviewed the mitohormetic response and assessed the berberine-induced effects and the possible signaling pathway involved. These findings may contribute to better clinical applications of berberine and indicate that some mitochondria-targeted conventional drugs should be considered carefully in clinical application.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The mitohormetic response as part of the cytoprotection mechanism of berberine

Zhu

Wei

Yang

et al. 2020

Mol Med

View full text Add to dashboard Cite

show abstract

“…Berberine ameliorated variety of diseases through mediating the autophagy [17]. Previous study presented that berberine decreased NLRP3 in ammasome activation by promoting autophagy in macrophages [18].…”

Section: Discussionmentioning

confidence: 94%

Berberine exhibits neuroprotective effects through inhibited autophagy and promoted microglial M1 transferred to M2 polarization

Qiang

Yang³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Intracerebral haemorrhage (ICH) induces autophagy excessive activation and microglia mainly switched into proinflammatory M1 type, which can cause severe secondary injury. Current evidence has implied that berberine has a protective effect against ischaemic stroke through mediated autophagy and microglial polarization. However, the neuroprotective effect of berberine in intracerebral hemorrhage (ICH) remains unclear.Method: In this study the effect of berberine on rats model of intracerebral hemorrhage were investigated through Immunofluorescence, qPCR, ELISA, and western blot.Result: Berberine administration significantly reduces neurological deficits and the brain water content via inhibited autophagy, promoted M1 type microglia to M2 type, and subsequently exerts anti-inflammation effects in a rat model of ICH.Conclusion: These results suggest that berberine reduced secondary injury and improved neurological outcomes in ICH model.

show abstract

“…A growing body of evidence has elucidated that ER stress takes part in the pathogenic processes of I/R injury [26]. Laboratory studies report that GRP78 and CRT, serving as key signaling molecules involved in ER stress-related pathways, are highly expressed in the tissues which suffer from I/R damage [27][28][29].…”

Section: Discussionmentioning

confidence: 99%

PERK Overexpression-Mediated Nrf2/HO-1 Pathway Alleviates Hypoxia/Reoxygenation-Induced Injury in Neonatal Murine Cardiomyocytes via Improving Endoplasmic Reticulum Stress

Wang

Lü

Chen

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

Reperfusion processes following acute myocardial infarction (AMI) have been reported to induce additional cardiomyocyte death, known as ischemia-reperfusion (I/R) injury. Endoplasmic reticulum (ER) stress is reported to be involved in the development of I/R injury. There is evidence that PERK exerts beneficial roles in alleviating ER stress. Here, we investigated whether upregulation of PERK improved cardiomyocytes injury induced by I/R. Specific siRNAs or adenovirus vectors were incubated with isolated neonatal cardiomyocytes (NCMs) to regulate expression levels of target genes including PERK, Nrf2, and HO-1. Afterwards, hypoxia and subsequent reoxygenation (H/R) administration was performed as the in vitro model of I/R injury. MTT assay showed that H/R intervention decreased the viability of cells, yet PERK overexpression increased the cellular proliferative rate. Moreover, the upregulation of Nrf2 or HO-1 elevated the growth rate of cells, while gene silencing of Nrf2 or HO-1 reduced the viability of NCMs treated with PERK-rAAV9. In addition, we observed that the apoptotic index of cells with H/R stimulation was reduced when NCMs were pretreated with PERK-rAAV9, Nrf2-rAAV9, or HO-1-rAAV9. After cells were incubated with Nrf2-siRNA or HO-1-siRNA, the upregulation of PERK had no roles in affecting the apoptosis rate of NCMs damaged by H/R. Then, our findings indicated that there was a level decrease of GRP78, CRT, CHOP, and Caspase-12 in NCMs of the PERK-rAAV9 group compared to that of the H/R group. Both Nrf2 overexpression and HO-1 upregulation reduced the expression of ER stress-related proapoptotic factors, yet the expression suppression of Nrf2 and HO-1 increased levels of GRP78, CRT, CHOP, and Caspase-12 in NCMs treated with PERK-rAAV9. Taken together, our results suggested that the effects of PERK against H/R injury might be attributed to the upregulation of Nrf2/HO-1 cascade, followed by the inhibition of ER stress-related apoptotic pathway.

show abstract

Berberine protects against ischemia-reperfusion injury: A review of evidence from animal models and clinical studies

Cited by 66 publications

References 74 publications

The mitohormetic response as part of the cytoprotection mechanism of berberine

The mitohormetic response as part of the cytoprotection mechanism of berberine

Berberine exhibits neuroprotective effects through inhibited autophagy and promoted microglial M1 transferred to M2 polarization

PERK Overexpression-Mediated Nrf2/HO-1 Pathway Alleviates Hypoxia/Reoxygenation-Induced Injury in Neonatal Murine Cardiomyocytes via Improving Endoplasmic Reticulum Stress

Contact Info

Product

Resources

About