Protective effects of aloperine on neonatal rat primary cultured hippocampal neurons injured by oxygen–glucose deprivation and reperfusion

Ma, Ning; Zhou, Ran; Chang, Ren-Yuan; Hao, Yinju; Ma, Lin; Jin, Shaoju; Du, Juan; Zheng, Jie; Zhao, Caidan; Niu, Yang; Sun, Tao; Li, Wei; Koike, Kazuo; Yu, Jian‐Qiang; Li, Yuxiang

doi:10.1007/s11418-015-0928-2

Cited by 32 publications

(31 citation statements)

References 24 publications

(23 reference statements)

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“…A 2016 study proposed aloperine and its derivatives as a new class of HIV-1 inhibitors [28] while a more recent study proposed the same as a new class of hepatitis C virus inhibitors [29]. Aloperine exerts a significant antioxidant effect by downregulating the production of ROS and increasing enzymatic activity and total antioxidant capacity in neuronal cells [30]. Another study demonstrated an anti-oxidative stress effect in an Alzheimer's model, where aloperine suppressed ROS and 4-hydroxy-2-nonenal production while increasing mitochondrial membrane potential and adenosine triphosphate production [31].…”

Section: Discussionmentioning

confidence: 99%

The protective effects of aloperine against ox-LDL-induced endothelial dysfunction and inflammation in HUVECs

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Atherosclerosis is a potentially life-threatening cardiovascular disease characterized by chronic endothelial inflammation and the formation of atherosclerotic lesions. Circulating ox-LDL is known to induce atherosclerosis by triggering oxidative stress, the expression of inflammatory mediators and adhesion molecules, as well as downregulating the atheroprotective transcriptional factor KLF2. Aloperine is an alkaloid compound isolated from the plant Sophora alopecuroides. Here, we employed various experimental methods to determine the effects of aloperine on ox-LDL-induced markers of atherosclerosis. DHE staining revealed that aloperine may restore the oxidant/antioxidant balance in HUVECs by reducing the level of ROS and rescuing the reduction in NOQ-1 and GCLC induced by ox-LDL. Aloperine treatment reduced ox-LDL-induced expression of IL-6, MCP-1, VCAM-1, and E-selectin and rescued the reduction in KLF2. Aloperine also downregulated ox-LDL-induced expression of the LOX-1. We also demonstrate that aloperine improved cell viability and inhibited the adhesion of U937 monocytes to HUVECs. Finally, we demonstrate that the effects of aloperine are mediated through the rescue of KLF2 expression via suppression of the phosphorylation of p53 protein. Together, our results implicate the potential of aloperine as a safe and effective antiatherosclerosis treatment.

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Section: Discussionmentioning

confidence: 99%

The protective effects of aloperine against ox-LDL-induced endothelial dysfunction and inflammation in HUVECs

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…The accumulated toxic metabolic products could inhibit mitochondrial ATP turnover in neuron cells, leading to “aged” mitochondria with impaired ATP production and increased ROS leakage (Martin et al, 2005). ROS is a well known factor contributing to brain I/R injury (Zeiger et al, 2009; Ma et al, 2015). During I/R, the brain activates its own protection mechanism IPC to remove the ROS generated by I/R injury.…”

Section: Discussionmentioning

confidence: 99%

“…The cultures were incubated under the condition of 95% N 2 and 5% CO 2 at 37°C for 2 h as OGD (Ma et al, 2015). …”

Section: Methodsmentioning

confidence: 99%

“…Even a short term of OGD can cause irreversibe damages to brain cells, while subsequent reperfusion, restoring blood supply to the brain, may aggravate the damage even further (Lin et al, 2016). Ischemia/reperfusion (I/R) induced oxidative stress, caused by impaired metabolism in the brain cells, is believed to be the one of the major contributors to brain I/R injury (Zeiger et al, 2009; Ma et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

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NaHS Protects against the Impairments Induced by Oxygen-Glucose Deprivation in Different Ages of Primary Hippocampal Neurons

Wang

Zhao

et al. 2017

Front. Cell. Neurosci.

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Brain ischemia leads to poor oxygen supply, and is one of the leading causes of brain damage and/or death. Neuroprotective agents are thus in great need for treatment purpose. Using both young and aged primary cultured hippocampal neurons as in vitro models, we investigated the effect of sodium hydrosulfide (NaHS), an exogenous donor of hydrogen sulfide, on oxygen-glucose deprivation (OGD) damaged neurons that mimick focal cerebral ischemia/reperfusion (I/R) induced brain injury. NaHS treatment (250 μM) protected both young and aged hippocampal neurons, as indicated by restoring number of primary dendrites by 43.9 and 68.7%, number of dendritic end tips by 59.8 and 101.1%, neurite length by 36.8 and 66.7%, and spine density by 38.0 and 58.5% in the OGD-damaged young and aged neurons, respectively. NaHS treatment inhibited growth-associated protein 43 downregulation, oxidative stress in both young and aged hippocampal neurons following OGD damage. Further studies revealed that NaHS treatment could restore ERK1/2 activation, which was inhibited by OGD-induced protein phosphatase 2 (PP2A) upregulation. Our results demonstrated that NaHS has potent protective effects against neuron injury induced by OGD in both young and aged hippocampal neurons.

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“…Further studies have shown that the inhibitory effect of apoptosis was related to antiinflammatory and down-regulation of MAPK signaling pathway (Zhao et al, 2017a). Similarly, aloperine (Ma et al, 2015), matrine, and oxymatrine (Zhao et al, 2015a;Zhao et al, 2015b; may have the same protective effect against ischemic neuron apoptosis. As a reversible selective inhibitor of true cholinesterase, huperzine A has been shown to inhibit mitochondrial complexes I-IV, a-ketoglutarate dehydrogenase, and MMP decline after ischemia, which helps to eliminating excessive ROS and Ca 2+ (Zheng et al, 2008).…”

Section: Monomers and Molecular Mechanisms In Regulating Mptp Opennesmentioning

confidence: 97%

Mitochondrial MPTP: A Novel Target of Ethnomedicine for Stroke Treatment by Apoptosis Inhibition

Sun

et al. 2020

Front. Pharmacol.

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Mammalian mitochondrial permeability transition pore (MPTP), across the inner and outer membranes of mitochondria, is a nonspecific channel for signal transduction or material transfer between mitochondrial matrix and cytoplasm such as maintenance of Ca 2+ homeostasis, regulation of oxidative stress signals, and protein translocation evoked by some of stimuli. Continuous MPTP opening has been proved to stimulate neuronal apoptosis in ischemic stroke. Meanwhile, inhibition of MPTP overopening-induced apoptosis has shown excellent efficacy in the treatment of ischemic stroke. Among of which, the potential molecular mechanisms of drug therapy for stroke has also been gradually revealed by researchers. The characteristics of multi-components or multitargets for ethnic drugs also provide the possibility to treat stroke from the perspective of mitochondrial MPTP. The advantages mentioned above make it necessary for us to explore and clarify the new perspective of ethnic medicine in treating stroke and to determine the specific molecular mechanisms through advanced technologies as much as possible. In this review, we attempt to uncover the relationship between abnormal MPTP opening and neuronal apoptosis in ischemic stroke. We further summarized currently authorized drugs, ethnic medicine prescriptions, herbs, and identified monomer compounds for inhibition of MPTP overopening-induced ischemic neuron apoptosis. Finally, we strive to provide a new perspective and enlightenment for ethnic medicine in the prevention and treatment of stroke by inhibition of MPTP overopeninginduced neuronal apoptosis.

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Protective effects of aloperine on neonatal rat primary cultured hippocampal neurons injured by oxygen–glucose deprivation and reperfusion

Cited by 32 publications

References 24 publications

The protective effects of aloperine against ox-LDL-induced endothelial dysfunction and inflammation in HUVECs

The protective effects of aloperine against ox-LDL-induced endothelial dysfunction and inflammation in HUVECs

NaHS Protects against the Impairments Induced by Oxygen-Glucose Deprivation in Different Ages of Primary Hippocampal Neurons

Mitochondrial MPTP: A Novel Target of Ethnomedicine for Stroke Treatment by Apoptosis Inhibition

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