Punicalagin exerts protective effect against high glucose-induced cellular stress and neural tube defects

Zhong, Jianxiang; Reece, E. Albert; Yang, Peixin

doi:10.1016/j.bbrc.2015.10.024

Cited by 50 publications

(30 citation statements)

References 38 publications

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“…We demonstrated that PUN pretreatment increased antioxidant enzyme SOD activity and reduced MDA formation following MI/R. These results indicate that PUN suppresses MI/R-induced oxidative stress, which is similar to previous studies that PUN attenuates oxidative stress in other diseases (Zhong et al, 2015;Rao et al, 2016).…”

Section: Discussionsupporting

confidence: 92%

Punicalagin Pretreatment Attenuates Myocardial Ischemia-Reperfusion Injury via Activation of AMPK

Ding

Sun

et al. 2017

Am. J. Chin. Med.

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Punicalagin (PUN), a major bioactive component in pomegranate juice, has been proven to exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) insult via anti-oxidant properties. This study aims to investigate whether PUN provides cardioprotection against myocardial I/R (MI/R) injury and the underlying mechanisms. PUN (30 mg/ kg/d) or vehicle was intragastrically administered to Sprague-Dawley rats for one week before the operation. MI/R was induced by ligating the left anterior descending coronary artery for 30 min and subsequent reperfusion for 3 h. PUN pretreatment conferred cardioprotective effects against MI/R injury by improving cardiac function, limiting infarct size, reducing serum creatine kinase-MB and lactate dehydrogenase activities, and suppressing cardiomyocyte apoptosis. Moreover, PUN pretreatment inhibited I/R-induced myocardial oxidative stress as evidenced by decreased generation of superoxide content and

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Section: Discussionsupporting

confidence: 92%

Punicalagin Pretreatment Attenuates Myocardial Ischemia-Reperfusion Injury via Activation of AMPK

Ding

Sun

et al. 2017

Am. J. Chin. Med.

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“…30,31,37,49,77 However, the effectiveness of these natural compounds needs be tested in human diabetic pregnancies.…”

Section: Commentmentioning

confidence: 99%

“…30,31 Epigallocatechin gallate is the major polyphenol in green tea ( Camellia sinensis ) and makes up to approximately 30% of the solids in green tea. 32 …”

mentioning

confidence: 99%

The green tea polyphenol EGCG alleviates maternal diabetes–induced neural tube defects by inhibiting DNA hypermethylation

Zhong

Reece

et al. 2016

American Journal of Obstetrics and Gynecology

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BACKGROUND Maternal diabetes increases the risk of neural tube defects in offspring. Our previous study demonstrated that the green tea polyphenol, Epigallocatechin gallate, inhibits high glucose-induced neural tube defects in cultured embryos. However, the therapeutic effect of Epigallocatechin gallate on maternal diabetes–induced neural tube defects is still unclear. OBJECTIVE We aimed to examine whether Epigallocatechin gallate treatment can reduce maternal diabetes–induced DNA methylation and neural tube defects. STUDY DESIGN Nondiabetic and diabetic pregnant mice at embryonic day 5.5 were given drinking water with or without 1 or 10 μM Epigallocatechin gallate. At embryonic day 8.75, embryos were dissected from the visceral yolk sac for the measurement of the levels and activity of DNA methyltransferases, the levels of global DNA methylation, and methylation in the CpG islands of neural tube closure essential gene promoters. embryonic day 10.5 embryos were examined for neural tube defect incidence. RESULTS Epigallocatechin gallate treatment did not affect embryonic development because embryos from nondiabetic dams treated with Epigallocatechin gallate did not exhibit any neural tube defects. Treatment with 1 μM Epigallocatechin gallate did not reduce maternal diabetes–induced neural tube defects significantly. Embryos from diabetic dams treated with 10 μM Epigallocatechin gallate had a significantly lower neural tube defect incidence compared with that of embryos without Epigallocatechin gallate treatment. Epigallocatechin gallate reduced neural tube defect rates from 29.5% to 2%, an incidence that is comparable with that of embryos from nondiabetic dams. Ten micromoles of Epigallocatechin gallate treatment blocked maternal diabetes–increased DNA methyltransferases 3a and 3b expression and their activities, leading to the suppression of global DNA hypermethylation. Additionally, 10 μM Epigallocatechin gallate abrogated maternal diabetes–increased DNA methylation in the CpG islands of neural tube closure essential genes, including Grhl3, Pax3, and Tulp3. CONCLUSION Epigallocatechin gallate reduces maternal diabetes–induced neural tube defects formation and blocks the enhanced expression and activity of DNA methyltransferases, leading to the suppression of DNA hypermethylation and the restoration of neural tube closure essential gene expression. These observations suggest that Epigallocatechin gallate supplements could mitigate the teratogenic effects of hyperglycemia on the developing embryo and prevent diabetes–induced neural tube defects.

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“…We have demonstrated that oxidative stress plays a causal role in PGDM-induced neural tube defects [12–14,16,49,58,60–63,67] and CHDs [48,50,52,57], and that overexpression of SOD1 in transgenic mice ameliorates PGDM-induced CHDs [48,50]. We previously reported that PGDM in vivo and high glucose in vitro decreased the expression of miR-322 in E8.5 embryos, and that overexpressing SOD1 restores miR-322 levels [19].…”

Section: Discussionmentioning

confidence: 99%

microRNA expression profiling and functional annotation analysis of their targets modulated by oxidative stress during embryonic heart development in diabetic mice

Dong

Zhang

Reece

et al. 2016

Reproductive Toxicology

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Maternal pregestational diabetes mellitus (PGDM) induces congenital heart defects (CHDs). The molecular mechanism underlying PGDM-induced CHDs is unknown. microRNAs (miRNAs), small non-coding RNAs, repress gene expression at the posttranscriptional level and play important roles in heart development. We performed a global miRNA profiling study to assist in revealing potential miRNAs modulated by PGDM and possible developmental pathways regulated by miRNAs during heart development. A total of 149 mapped miRNAs in the developing heart were significantly altered by PGDM. Bioinformatics analysis showed that the majority of the 2111 potential miRNA target genes were associated with cardiac development-related pathways including STAT3 and IGF-1 and transcription factors (Cited2, Zeb2, Mef2c, Smad4 and Ets1). Overexpression of the antioxidant enzyme, superoxide dismutase 1, reversed PGDM-altered miRNAs, suggesting that oxidative stress is responsible for dysregulation of miRNAs. Thus, our study provides the foundation for further investigation of a miRNA-dependent mechanism underlying PGDM-induced CHDs.

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Punicalagin exerts protective effect against high glucose-induced cellular stress and neural tube defects

Cited by 50 publications

References 38 publications

Punicalagin Pretreatment Attenuates Myocardial Ischemia-Reperfusion Injury via Activation of AMPK

Punicalagin Pretreatment Attenuates Myocardial Ischemia-Reperfusion Injury via Activation of AMPK

The green tea polyphenol EGCG alleviates maternal diabetes–induced neural tube defects by inhibiting DNA hypermethylation

microRNA expression profiling and functional annotation analysis of their targets modulated by oxidative stress during embryonic heart development in diabetic mice

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