Neuroprotective effects of pinocembrin on ischemia/reperfusion-induced brain injury by inhibiting autophagy

Tao, Jinhao; Shen, Chen; Sun, Yanchun; Chen, Wei-Ming; Yan, Gangfeng

doi:10.1016/j.biopha.2018.07.026

Cited by 61 publications

(41 citation statements)

References 44 publications

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“…Pinocembrin has been extensively studied due to its positive effects on cardiovascular system. This flavanone protects endothelial cells from oxidized LDL-induced injury, and has neuroprotective effects on ischemia/reperfusion-induced brain injury by inhibiting autophagy [ 36 , 37 ]. Although pharmacokinetic of pinocembrin was studied, no CYP3A4 inhibition was reported [ 38 ].…”

Section: Resultsmentioning

confidence: 99%

The Inhibitory Effect of Flavonoid Aglycones on the Metabolic Activity of CYP3A4 Enzyme

et al. 2018

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Flavonoids are natural compounds that have been extensively studied due to their positive effects on human health. There are over 4000 flavonoids found in higher plants and their beneficial effects have been shown in vitro as well as in vivo. However, data on their pharmacokinetics and influence on metabolic enzymes is scarce. The aim of this study was to focus on possible interactions between the 30 most commonly encountered flavonoid aglycones on the metabolic activity of CYP3A4 enzyme. 6β-hydroxylation of testosterone was used as marker reaction of CYP3A4 activity. Generated product was determined by HPLC coupled with diode array detector. Metabolism and time dependence, as well as direct inhibition, were tested to determine if inhibition was reversible and/or irreversible. Out of the 30 flavonoids tested, 7 significantly inhibited CYP3A4, most prominent being acacetin that inhibited 95% of enzyme activity at 1 µM concentration. Apigenin showed reversible inhibition, acacetin, and chrysin showed combined irreversible and reversible inhibition while chrysin dimethylether, isorhamnetin, pinocembrin, and tangeretin showed pure irreversible inhibition. These results alert on possible flavonoid–drug interactions on the level of CYP3A4.

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Section: Resultsmentioning

confidence: 99%

The Inhibitory Effect of Flavonoid Aglycones on the Metabolic Activity of CYP3A4 Enzyme

et al. 2018

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“…Taken together, all these findings suggest that propolis displays neuroprotective through multiple pathways which might be attributed by the presence of bioactive compounds in propolis as well as their combination of multitarget compound acting on the different pathways. Several studies have reported on the neuroprotective effect of compounds present in the propolis in various study models of neurodegenerative diseases; for example, kaempferol [80,83], chrysin [84], pinocembrin [85][86][87][88][89][90][91][92][93][94][95][96], and caffeic acid phenethyl ester [97][98][99][100][101][102][103][104][105][106][107][108]. ese studies reported and suggested that these bioactive compounds may protect against neurodegenerative characteristics of neurodegenerative diseases Evidence-Based Complementary and Alternative Medicine and the multiple mechanisms of the neuroprotective effect of compounds tested could be potentially involved.…”

Section: Neuroprotective Activities Of Natural Products and Their Biomentioning

confidence: 99%

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

Sairazi

Sirajudeen

2020

Evidence-Based Complementary and Alternative Medicine

130

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In recent years, natural products, which originate from plants, animals, and fungi, together with their bioactive compounds have been intensively explored and studied for their therapeutic potentials for various diseases such as cardiovascular, diabetes, hypertension, reproductive, cancer, and neurodegenerative diseases. Neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis are characterized by the progressive dysfunction and loss of neuronal structure and function that resulted in the neuronal cell death. Since the multifactorial pathological mechanisms are associated with neurodegeneration, targeting multiple mechanisms of actions and neuroprotection approach, which involves preventing cell death and restoring the function to damaged neurons, could be promising strategies for the prevention and therapeutic of neurodegenerative diseases. Natural products have emerged as potential neuroprotective agents for the treatment of neurodegenerative diseases. This review focused on the therapeutic potential of natural products and their bioactive compounds to exert a neuroprotective effect on the pathologies of neurodegenerative diseases.

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“…It has various biological functions such as anti-inflammatory, antioxidation, and antibacterial [ 3 ]. Previous studies have confirmed that pinocembrin confers neuroprotective effects during cerebral ischemic I/R [ 4 – 6 ]. Recent research has also tried to determine whether pinocembrin is beneficial for cardiac injury.…”

Section: Introductionmentioning

confidence: 81%

Cardioprotective Natural Compound Pinocembrin Attenuates Acute Ischemic Myocardial Injury via Enhancing Glycolysis

Zheng

Wan

Yang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Purpose. Emerging evidence has shown that pinocembrin protects the myocardium from ischemic injury in animals. However, it is unknown whether it has cardioprotection when given at the onset of reperfusion. Also, mechanisms mediating the cardioprotective actions of pinocembrin were largely unknown. Thus, this study is aimed at investigating the effects of pinocembrin postconditioning on ischemia-reperfusion (I/R) injury and the underlying mechanisms. Methods. The in vivo mouse model of myocardial I/R injury, ex vivo isolated rat heart with global I/R, and in vitro hypoxia/reoxygenation (H/R) injury model for primary cardiomyocytes were used. Results. We found that pinocembrin postconditioning significantly reduced the infarct size and improved cardiac contractile function after acute myocardial I/R. Mechanically, in primary cardiomyocytes, we found that pinocembrin may confer protection in part via direct stimulation of cardiac glycolysis via promoting the expression of the glycolytic enzyme, PFKFB3. Besides, PFKFB3 inhibition abolished pinocembrin-induced glycolysis and protection in cardiomyocytes. More importantly, PFKFB3 knockdown via cardiotropic adeno-associated virus (AAV) abrogated cardioprotective effects of pinocembrin. Moreover, we demonstrated that HIF1α is a key transcription factor driving pinocembrin-induced PFKFB3 expression in cardiomyocytes. Conclusions. In conclusion, these results established that the acute cardioprotective benefits of pinocembrin are mediated in part via enhancing PFKFB3-mediated glycolysis via HIF1α, which may provide a new therapeutic target to impede the progression of myocardial I/R injury.

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Neuroprotective effects of pinocembrin on ischemia/reperfusion-induced brain injury by inhibiting autophagy

Cited by 61 publications

References 44 publications

The Inhibitory Effect of Flavonoid Aglycones on the Metabolic Activity of CYP3A4 Enzyme

The Inhibitory Effect of Flavonoid Aglycones on the Metabolic Activity of CYP3A4 Enzyme

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

Cardioprotective Natural Compound Pinocembrin Attenuates Acute Ischemic Myocardial Injury via Enhancing Glycolysis

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