Limits...
Molecular targets for anti-oxidative protection of green tea polyphenols against myocardial ischemic injury.

Hsieh SR, Cheng WC, Su YM, Chiu CH, Liou YM - Biomedicine (Taipei) (2014)

Bottom Line: An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway.Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury.Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Surgery, Taichung Veterans General Hospital, 407 Taichung, Taiwan.

ABSTRACT

Ischemic heart disease is the leading cause of death worldwide. An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway. Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury. Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed. Proteomics analyses widely used to identify the protein targets for many cardiovascular diseases have advanced the discovery of the signaling mechanism for GTPs-mediated cardio-protection. This review focuses on putative triggers, mediators, and end effectors for the GTPs-mediated cardio-protection signaling pathways engaged in myocardial ischemia crisis, allowing a promising natural product to be used for ameliorating oxidative stress associated with ischemic heart diseases.

No MeSH data available.


Related in: MedlinePlus

Myocardial ischemia models of chronic myocardial infarction (MI) and transient ischemia-reperfusion (IR) created in rats by ligating the left anterior descending coronary (LAD).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4264984&req=5

Fig1: Myocardial ischemia models of chronic myocardial infarction (MI) and transient ischemia-reperfusion (IR) created in rats by ligating the left anterior descending coronary (LAD).

Mentions: Two different myocardial ischemia models (Figure 1) associated with chronic myocardial infarction (MI) and transient ischemiareperfusion (IR) were created in rats by ligating the left anterior descending coronary (LAD) for studying myocardial ischemic injury [13, 14]. In the MI model, severe myocardial infarction was found in post-MI rats [14], while the IR model involving brief regional ischemia for 20 min followed by subsequent reperfusion showed no severe infarcted injury [13]. These findings suggested that brief regional ischemia followed reperfusion may lead to activate pathways that either preserve cell viability (preconditioning) or lead to cell death (IR injury). In contrast, irreversible MI caused by death of myocytes, presumably as a result of both necrosis and apoptosis, mostly appears within the infarct and periinfarct regions [32-35].


Molecular targets for anti-oxidative protection of green tea polyphenols against myocardial ischemic injury.

Hsieh SR, Cheng WC, Su YM, Chiu CH, Liou YM - Biomedicine (Taipei) (2014)

Myocardial ischemia models of chronic myocardial infarction (MI) and transient ischemia-reperfusion (IR) created in rats by ligating the left anterior descending coronary (LAD).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4264984&req=5

Fig1: Myocardial ischemia models of chronic myocardial infarction (MI) and transient ischemia-reperfusion (IR) created in rats by ligating the left anterior descending coronary (LAD).
Mentions: Two different myocardial ischemia models (Figure 1) associated with chronic myocardial infarction (MI) and transient ischemiareperfusion (IR) were created in rats by ligating the left anterior descending coronary (LAD) for studying myocardial ischemic injury [13, 14]. In the MI model, severe myocardial infarction was found in post-MI rats [14], while the IR model involving brief regional ischemia for 20 min followed by subsequent reperfusion showed no severe infarcted injury [13]. These findings suggested that brief regional ischemia followed reperfusion may lead to activate pathways that either preserve cell viability (preconditioning) or lead to cell death (IR injury). In contrast, irreversible MI caused by death of myocytes, presumably as a result of both necrosis and apoptosis, mostly appears within the infarct and periinfarct regions [32-35].

Bottom Line: An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway.Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury.Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Surgery, Taichung Veterans General Hospital, 407 Taichung, Taiwan.

ABSTRACT

Ischemic heart disease is the leading cause of death worldwide. An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway. Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury. Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed. Proteomics analyses widely used to identify the protein targets for many cardiovascular diseases have advanced the discovery of the signaling mechanism for GTPs-mediated cardio-protection. This review focuses on putative triggers, mediators, and end effectors for the GTPs-mediated cardio-protection signaling pathways engaged in myocardial ischemia crisis, allowing a promising natural product to be used for ameliorating oxidative stress associated with ischemic heart diseases.

No MeSH data available.


Related in: MedlinePlus