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July 26, 2016Scientific ReportsOpen Access

Standardized Chinese Formula Xin-Ke-Shu inhibits the myocardium Ca2+ overloading and metabolic alternations in isoproterenol-induced myocardial infarction rats

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Key result

Xin-Ke-Shu significantly reversed the over-expressions of PLA2 IIA, CaMK II, and Pro-Caspase-3 and regulated metabolic perturbations in isoproterenol-induced myocardial infarction rats.

Why the study?

Does Xin-Ke-Shu inhibit myocardium Ca2+ overloading and metabolic alterations in isoproterenol-induced myocardial infarction models?

Population

Isoproterenol (ISO)-induced myocardial infarction (MI) rats and H9c2 cells

Comparison

Xin-Ke-Shu pretreatment vs Normal control, ISO-induced MI model without…

Design

Preclinical

Authors

YLYuetao LiuShanxi UniversityCZChao ZhouQingdao UniversityHJHong‐Mei JiaChinese Academy of Medical Sciences & Peking Union Medical College

Discussion

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Implication

Hypothesis-generating for Xin-Ke-Shu in isoproterenol-induced MI models; does not yet inform clinical practice.

Structured PICO

Does Xin-Ke-Shu inhibit myocardium Ca2+ overloading and metabolic alterations in isoproterenol-induced myocardial infarction models?

P
Population
24 male Wistar rats with isoproterenol-induced myocardial infarction treated with Xin-Ke-Shu or controls for 4 weeks.
I
Intervention
Xin-Ke-Shu (XKS) pretreatment (oral administration in rats; 0.0625, 0.125, and 0.25 mg/mL in H9c2 cells)
C
Comparator
Normal control, ISO-induced MI model without XKS, and propranolol treatment
O
Outcome
Myocardial metabolic profiles and expression of PLA2 IIA, CaMK II, and Pro-Caspase-3surrogate

Main Result

p-value: p=<0.05

Xin-Ke-Shu protects against isoproterenol-induced myocardial infarction in preclinical models by inhibiting the Ca2+ overloading mechanism and regulating associated metabolic pathways.

Limitations

  • Confirmation of active ingredients' direct inhibition of Ca2+ overloading is further required

Cite This Study

Liu et al. (2016) studied Isoproterenol-induced myocardial infarction (n=24). Xin-Ke-Shu vs. Isoproterenol alone was evaluated on Expressions of PLA2 IIA, CaMK II and Pro-Caspase-3 (p=<0.05). Xin-Ke-Shu significantly reversed the over-expressions of PLA2 IIA, CaMK II, and Pro-Caspase-3 and regulated metabolic perturbations in isoproterenol-induced myocardial infarction rats.

synapsesocial.com/papers/6a9f63296b2f41ee0d04ed77https://doi.org/10.1038/srep30208
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