Eriodictyol Attenuates Myocardial Ischemia-Reperfusion Injury through the Activation of JAK2

Li, Defang; Lü, Nonghua; Han, Jichun; Chen, Xiaoyu; Wu, Hao; Xu, Wenjuan; Liu, Xiaona; Ye, Lei; Zheng, Qiusheng

doi:10.3389/fphar.2018.00033

Cited by 30 publications

(26 citation statements)

References 31 publications

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“…Eriodictyol is a natural flavonoid compound. Previous studies have shown that eriodictyol exerts anti-inflammatory and antioxidant effects both in vitro and in vivo (Li et al, 2018;He et al, 2019). However, the effects of eriodictyol on cancer and its underlying mechanisms largely remain unexplored.…”

Section: Discussionmentioning

confidence: 99%

Eriodictyol Inhibits Proliferation, Metastasis and Induces Apoptosis of Glioma Cells via PI3K/Akt/NF-κB Signaling Pathway

et al. 2020

Front. Pharmacol.

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Glioma is the most common type of malignant brain tumor. Due to its highly aggressive and metastatic features, glioma is associated with poor prognosis and a lack of effective treatments. Eriodictyol, a natural flavonoid compound, has been reported to possess antiinflammatory and antioxidant effects. However, the anti-tumor effects of eriodictyol and the underlying mechanisms have rarely been reported. In this study, we found that eriodictyol has anti-tumor activity in lung, colon, breast, pancreas, and liver cancer, and most significantly in glioma cell lines. Eriodictyol dose-and time-dependently suppresses cell proliferation, migration, and invasion in U87MG and CHG-5 glioma cells. In addition, eriodictyol induces apoptosis in U87MG and CHG-5 cells, as evaluated by flow cytometry, immunofluorescence, and Western blot. Furthermore, eriodictyol downregulates the phosphoinositide 3-kinase (PI3K)/Akt/NF-kB signaling pathway in a concentrationdependent manner. Moreover, the effects of eriodictyol on the apoptosis of glioma cells are enhanced by LY294002 (a PI3K inhibitor) and reversed by 740 Y-P (a PI3K agonist). In a mouse xenograft model, eriodictyol not only dramatically suppressed tumor growth but also induced apoptosis in tumor cells. In summary, our data illustrate that eriodictyol effectively inhibits proliferation and metastasis and induces apoptosis of glioma cell lines, which might be a result of the blockade of the PI3K/Akt/NF-kB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Eriodictyol Inhibits Proliferation, Metastasis and Induces Apoptosis of Glioma Cells via PI3K/Akt/NF-κB Signaling Pathway

et al. 2020

Front. Pharmacol.

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“…Due to the essential role of oxidative stress and inflammatory responses in the pathogenesis of myocardial infarction [ 9 , 12 ], antioxidant stress and anti-inflammatory responses present novel strategies on harmful event prevention and myocardial dysfunction attenuation [ 14 , 15 ]. Therefore, the current study determined the effects of HXP treatment on serum levels of antioxidant enzyme SOD, the lipid peroxidation marker MDA, and proinflammatory cytokines (IL-6 and TNF- α ).…”

Section: Discussionmentioning

confidence: 99%

“…When inflammatory response occurs after myocardial infarction, inflammatory cytokines are released and the numbers of macrophages gradually increase, provoking further myocardial damage [ 13 ]. However, antioxidant stress response and anti-inflammatory may prevent these harmful events and attenuate myocardial dysfunctions [ 14 , 15 ]. In the pathophysiological processes of myocardial ischemia, heart injury can be aggravated due to the large number of inflammatory factors and oxygen free radicals [ 16 ], leading to critical syndromes such as arrhythmia and heart failure, and initiating the activation of many signaling pathways [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Huoxin Pill Attenuates Cardiac Inflammation by Suppression of TLR4/NF‐κB in Acute Myocardial Ischemia Injury Rats

Chu

Zhou

Peng

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Huoxin Pill (HXP), a traditional Chinese medicine, has been prescribed widely in the treatment of coronary heart disease, angina pectoris, and other diseases. However, the possible protective mechanisms of HXP on myocardial ischemia remain unclear. In the current study, we investigated the effects and potential mechanism of HXP on myocardial ischemia and cardiac inflammation and the activation of TLR4/NF-κB pathway. Determination of electrocardiogram, echocardiography, and heart weight index (HWI) indicated that HXP treatment obviously attenuated the elevation of ST-segment, end-diastolic volume, and HWI in the AMI rat model. Enzyme-linked immunosorbent assay (ELISA) demonstrated that Huoxin Pill treatment significantly decreased the levels of CTnT, CK-MB, MDA, IL-6, and TNF-α, while it increased SOD content in serum of the AMI rat model. Moreover, hematoxylin and eosin (HE) and immunohistochemistry (IHC) staining revealed that HXP treatment alleviated pathological change, infiltration of inflammatory cells, levels of IL-6 and TNF-α, and expression of TLR4 and p-NF-κB in cardiac tissues of the AMI rat model. In conclusion, HXP treatment significantly improves cardiac function and attenuates cardiac inflammation by suppressing the activation of TLR4/NF-κB pathway in the ISO-induced AMI rat model. This study provides insights into the potential of HXP on prevention and treatment of AMI.

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“…JAK2 is a member of the JAK kinase family. Many studies have shown that JAK2 expression or functional changes are related to I-R injury in various organs such as myocardium [10], brain [11], and kidney [7]. MicroRNA (miRNA) is a class of single-stranded, noncoding RNA molecules made up of 22–25 nucleotides.…”

Section: Introductionmentioning

confidence: 99%

“…Studies have shown that apigenin is closely related to JAK2-STAT3 pathway activity and ischemia-reperfusion injury [22]. The activity of the JAK2-STAT3 pathway is closely related to injury to the heart [8,10,12], kidneys [7,9], and brain [11]. Luo found that osthole reduced renal reperfusion injury by regulating JAK2-STAT3 pathway activity [7].…”

Section: Introductionmentioning

confidence: 99%

Apigenin Alleviates Myocardial Reperfusion Injury in Rats by Downregulating miR-15b

Wang

Sun

et al. 2019

Med Sci Monit

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Background We investigated whether apigenin could mitigate myocardial reperfusion injury in rats, and a possible mechanism was proposed. Material/Methods The I-R injury model was established in rats along with a sham group as control, and the expressions of microRNA-15b (miR-15b), JAK2, and p-JAK2 in the myocardia of the 2 groups were detected. Apoptosis and reactive oxygen species (ROS) were also detected. Rats in the I-R injury model were divided into 3 groups in vivo : the 1I-R group, the 2I-R+solvent group, and the 3I-R+apigenin group. Expression of miR-15b, JAK2, p-JAK2, STAT3, and p-STAT3 in the myocardia of the 3 groups were detected. ROS content, apoptosis, MDA content, SOD, and CAT activities were detected. Rat myocardial H9C2 cells were cultured in vitro and divided into 5 treatment groups in vitro; expressions of miR-15b, JAK2, p-JAK2, STAT3, and p-STAT3 in H9C2 cells were detected, and the apoptosis and ROS content were detected by flow cytometry. Results We found that the increased miR-15b expression during myocardial I-R injury in rats downregulated the expression of JAK2 and activity of the JAK2-STAT3 pathway, promoted myocardial apoptosis and ROS production, and aggravated myocardial I-R injury. Apigenin treatment can downregulate miR-15b expression, increase the expression of JAK2 and the activity of JAK2-STAT3 pathway, reduce myocardial apoptosis and ROS production, and alleviate myocardial I-R injury. Conclusions Api treatment downregulated the expression of miR-15b and upregulated the expression of JAK2 and the activity of the JAK2-STAT3 pathway, thereby alleviating myocardial I-R injury, cardiomyocyte apoptosis, and ROS production in vitro .

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Eriodictyol Attenuates Myocardial Ischemia-Reperfusion Injury through the Activation of JAK2

Cited by 30 publications

References 31 publications

Eriodictyol Inhibits Proliferation, Metastasis and Induces Apoptosis of Glioma Cells via PI3K/Akt/NF-κB Signaling Pathway

Eriodictyol Inhibits Proliferation, Metastasis and Induces Apoptosis of Glioma Cells via PI3K/Akt/NF-κB Signaling Pathway

Huoxin Pill Attenuates Cardiac Inflammation by Suppression of TLR4/NF‐κB in Acute Myocardial Ischemia Injury Rats

Apigenin Alleviates Myocardial Reperfusion Injury in Rats by Downregulating miR-15b

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