Apigenin attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage

Han, Yuwei; Zhang, Tingting; Su, Jingyuan; Zhao, Yuan; Chenchen,; Wang, Hong; Li, Xiaoming

doi:10.1016/j.jocn.2017.03.003

Cited by 60 publications

(40 citation statements)

References 30 publications

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“…apigenin is a natural product in various chinese herbs and exhibits high bioactivity, including anticancer, antiinflammatory, and antifibrotic effects (27)(28)(29). In addition, previous studies have indicated that it also elicits neuroprotective effects (30,31). in the present study, depressive-like mice, induced by chronic restraint stress, were used to investigate the antidepressant effects of apigenin.…”

Section: Discussionmentioning

confidence: 93%

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

Zhang

Jiang

et al. 2019

Mol Med Report

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The present study aimed to investigate whether apigenin elicits antidepressant effects in depressant-like mice via the regulation of autophagy. The depressant-like behaviors were established in a chronic restraint stress model. Male BalB/c mice were subjected to restraint stress for 6 h/day for a period of 21 days, and deficits in sucrose preference, tail suspension and forced swim tests were confirmed to be improved following oral apigenin. To investigate the underlining mechanisms, the hippocampal levels of p62 and microtubule-associated protein light chain 3-ii/i (lc3-ii/i) were measured using western blot analysis. The expression levels of lc3-ii/i and p62 indicated that the significantly inhibited autophagy level induced by chronic restraint stress can be increased following apigenin treatment. Similar to the level of autophagy, the expression levels of adenosine monophosphate-activated protein kinase (aMPK) and unc-51 like autophagy activating kinase-1 were downregulated after chronic restraint stress stimulation and, subsequently upregulated following treatment with apigenin. conversely, the levels of mammalian target of rapamycin (mTor) were increased in chronic restraint stress mice and inhibited by apigenin. Collectively, the present findings indicated that apigenin potentially promotes autophagy via the aMPK/mTor pathway and induces antidepressive effects in chronic restraint stress mice.

show abstract

Section: Discussionmentioning

confidence: 93%

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

Zhang

Jiang

et al. 2019

Mol Med Report

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show abstract

“…The present results demonstrated that apigenin had limited cytotoxicity to H9C2 cells. Previous studies suggested that apigenin exhibits the function of suppressing oxidative stress in early brain injury and Parkinson's disease ( 34 , 35 ). LDH, MDA and CAT are considered to represent oxidative stress markers, and are involved in the regulation of the intracellular redox state ( 36 ).…”

Section: Discussionmentioning

confidence: 99%

Apigenin suppresses the apoptosis of H9C2 rat cardiomyocytes subjected to myocardial ischemia‑reperfusion injury via upregulation of the PI3K/Akt pathway

et al. 2018

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Apigenin, a flavonoid with multiple physiological and pharmacological activities, is associated with the prevention of cardiovascular diseases. The present study aimed to examine the roles and mechanisms of apigenin in the apoptosis of H9C2 rat cardiomyocytes, which were subjected to myocardial ischemia-reperfusion (MI/R) injury. Cell viability, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and cellular apoptosis were evaluated using cell counting kit-8 assays and flow cytometry. The content/activity of oxidative stress markers was determined using commercial kits. Western blot analysis and reverse transcription-quantitative polymerase chain reaction assays were used to measure protein and mRNA expression, respectively. The results demonstrated that apigenin had limited cytotoxicity on the viability of H9C2 rat cardiomyocytes. Apigenin reduced the oxidative stress, ROS production and cellular apoptotic capacity of MI/R-induced H9C2 cells. Apigenin additionally increased the MMP level of MI/R-induced H9C2 cells. Furthermore, apigenin modulated apoptosis-associated protein expression and phosphatidylinositol 3′-kinase (PI3K)/RAC-α serine/threonine-protein kinase (Akt) signaling in MI/R-induced H9C2 cells. Treatment with LY294002 reversed the anti-apoptotic effect of apigenin. In conclusion, apigenin suppressed the apoptosis of H9C2 cells that were subjected to MI/R injury by activating the PI3K/Akt pathway. It was suggested that apigenin may be effective as an MI/R therapy.

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“…It has been reported that hyperglycemia can cause increased neuronal damage in hippocampus of SAH, resulting in increased neuronal necrosis and increased infarction size ( 10 , 11 ). In the event of SAH, apoptosis of a variety of types of cells, such as vascular endothelial cells ( 12 ), neuronal cells ( 13 ) and other cells will occur. Caspase-3, which is the convergence point of the apoptotic signaling pathway, is a common part of various apoptotic signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Expression of caspase-3, Bax and Bcl-2 in hippocampus of rats with diabetes and subarachnoid hemorrhage

Jian-kui

Huang

2017

Exp Ther Med

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The expression of caspase-3, Bax and Bcl-2 in hippocampus of rats with diabetes and subarachnoid hemorrhage (SAH) were investigated. Diabetes mellitus model was established by intraperitoneal injection of STZ. On the basis of diabetes mellitus model, SAH animal model was established by injecting fresh autologous femoral artery blood into cerebellomedullary cisten. Rats were divided into blank control group, diabetes control group and diabetes + SAH group. TUNEL method was used to detect cell apoptosis of hippocampus. Expression levels of caspase-3, Bax and Bcl-2 were detected by real-time quantitative reverse transcription PCR and western blot analysis at mRNA and protein levels, respectively. Apoptotic cells were not detected in blank control group and diabetes group, and number of apoptotic cells was the highest in the diabetic SAH group. Expression levels of caspase-3, Bax and Bcl-2 mRNA and protein were significantly higher in diabetes + SAH group than in blank control group and diabetes group. In conclusion, Hippocampal neuron apoptosis was induced by diabetes + SAH and expression levels of caspase-3, Bax and Bcl-2 were also increased. Our study provided experimental basis for further studies of the relationship between SAH and cell apoptosis.

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Apigenin attenuates oxidative stress and neuronal apoptosis in early brain injury following subarachnoid hemorrhage

Cited by 60 publications

References 30 publications

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

Apigenin suppresses the apoptosis of H9C2 rat cardiomyocytes subjected to myocardial ischemia‑reperfusion injury via upregulation of the PI3K/Akt pathway

Expression of caspase-3, Bax and Bcl-2 in hippocampus of rats with diabetes and subarachnoid hemorrhage

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