Puerarin protected the brain from cerebral ischemia injury via astrocyte apoptosis inhibition

Wang, Nan; Zhang, Yanmin; Wu, Lei; Wang, Yuanji; Cao, Yanjun; He, Langchong; Li, Xia; Zhao, Jianjun

doi:10.1016/j.neuropharm.2013.12.004

Cited by 88 publications

(67 citation statements)

References 34 publications

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“…The mNSS is a composite of motor, sensory, balance and reflex tests with the maximum scores of 6, 2, 6, and 4 points, respectively. Thus, higher scores indicate more severe neurological dysfunction (13–18 = severe, 7–12 = moderate, and 1–6 = mild) 44 .…”

Section: Methodsmentioning

confidence: 99%

Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury

Yang¹,

Yi²,

Zhang³

et al. 2017

Sci Rep

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Necroptosis, a novel type of programmed cell death, is involved in stroke-induced ischemic brain injury. Although studies have sought to explore the mechanisms of necroptosis, its signaling pathway has not yet to be completely elucidated. Thus, we used oxygen-glucose deprivation (OGD) and middle cerebral artery occlusion (MCAO) models mimicking ischemic stroke (IS) conditions to investigate mechanisms of necroptosis. We found that OGD and MCAO induced cell death, local brain ischemia and neurological deficit, while zVAD-fmk (zVAD, an apoptotic inhibitor), GSK’872 (a receptor interacting protein kinase-3 (RIP3) inhibitor), and combined treatment alleviated cell death and ischemic brain injury. Moreover, OGD and MCAO upregulated protein expression of the triggers of necroptosis: receptor interacting protein kinase-1 (RIP1), RIP3 and mixed lineage kinase domain-like protein (MLKL). The upregulation of these proteins was inhibited by GSK’872, combination treatments and RIP3 siRNA but not zVAD treatment. Intriguingly, hypoxia-inducible factor-1 alpha (HIF-1α), an important transcriptional factor under hypoxic conditions, was upregulated by OGD and MCAO. Similar to their inhibitory effects on aforementioned proteins upregulation, GSK’872, combination treatments and RIP3 siRNA decreased HIF-1α protein level. These findings indicate that necroptosis contributes to ischemic brain injury induced by OGD and MCAO and implicate HIF-1α, RIP1, RIP3, and MLKL in necroptosis.

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Section: Methodsmentioning

confidence: 99%

Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury

Yang¹,

Yi²,

Zhang³

et al. 2017

Sci Rep

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“…In this regard, selectins and CAMs are the most relevant molecules involved in the adhesion process (Stanimirovic and Satoh 2000;Wang et al 2007;Petri et al 2008). In an attempt to estimate the role of neuroinflammation in apoptosis, we used the effector cleaved caspase-3, which is considered the main marker in apoptosis (He et al 2006;Wang et al 2013;Fan et al 2014). …”

Section: Selection Of Times and Markersmentioning

confidence: 99%

Age-dependent modifications in vascular adhesion molecules and apoptosis after 48-h reperfusion in a rat global cerebral ischemia model

Anuncibay‐Soto

Pérez‐Rodríguez

Llorente

et al. 2014

AGE

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Stroke is one of the leading causes of death and permanent disability in the elderly. However, most of the experimental studies on stroke are based on young animals, and we hypothesised that age can substantially affect the stroke response. The two-vessel occlusion model of global ischemia by occluding the common carotid arteries for 15 min at 40 mmHg of blood pressure was carried out in 3-and 18-month-old male Sprague-Dawley rats. The adhesion molecules E-and P-selectin, cell adhesion molecules (CAMs), both intercellular (ICAM-1) and vascular (VCAM-1), as well as glial fibrillary acidic protein (GFAP), and cleaved caspase-3 were measured at 48 h after ischemia in the cerebral cortex and hippocampus using Western blot, qPCR and immunofluorescence techniques. Diametric expression of GFAP and a different morphological pattern of caspase-3 labelling, although no changes in the cell number, were observed in the neurons of young and old animals. Expression of E-selectin and CAMs was also modified in an age-and ischemia/reperfusiondependent manner. The hippocampus and cerebral cortex had similar response patterns for most of the markers studied. Our data suggest that old and young animals present different time-courses of neuroinflammation and apoptosis after ischemic damage. On the other hand, these results suggest that neuroinflammation is dependent on age rather than on the different vulnerability described for the hippocampus and cerebral cortex. These differences should be taken into account in searching for therapeutic targets.

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“…Puerarin (C 21 H 20 O 9 ) is an isoflavone glycoside that is extracted from the root of the wild leguminous creeper Pueraria lobata and has been widely used to treat myocardial infarction, cerebral ischemia, cancer, and osteoporosis, and diabetic nephropathy in China [14]. Puerarin has also been reported to possess different biological activities including anti-oxidation, anti-inflammation, anti-apoptosis, and neuroprotection [15][16][17]. Song et al [18] reported that puerarin can restore mitochondrial function and protect tubular cell from apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Puerarin Attenuates Osteoarthritis via Upregulating AMP-Activated Protein Kinase/Proliferator-Activated Receptor-γ Coactivator-1 Signaling Pathway in Osteoarthritis Rats

et al. 2018

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Background/Aims: Osteoarthritis is the most common degenerative joint disease and causes major pain and disability in adults. It has been reported that mitochondrial dysfunction in chondrocytes was associated with osteoarthritis. Puerarin has multiple effects including restoring mitochondrial function. In this study, the potential effects of puerarin on osteoarthritis and osteoarthritis associated mitochondrial dysfunctions were evaluated. Methods: Osteoarthritis rats were treated with puerarin and the severity of osteoarthritis and cartilage damages was evaluated. The mitochondrial biogenesis and functions were analyzed by measuring related proteins expression, mitochondrial DNA content, ATP production, and oxygen consumption. The dependence of AMP-activated protein kinase (AMPK) pathway on puerarin-regulated mitochondrial function was analyzed by applying AMPK inhibitor Compound C. Results: Puerarin treatment alleviated mechanical hyperalgesia and cartilage damage in osteoarthritis rats. Puerarin increased mitochondrial biogenesis and attenuated mitochondrial dysfunctions in osteoarthritis rats. AMPK inhibitor Compound C abolished puerarin’s effects. Conclusion: Puerarin attenuates osteoarthritis by upregulating the AMPK/proliferator-activated receptor-γ coactivator signaling pathway in osteoarthritis rats.

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Puerarin protected the brain from cerebral ischemia injury via astrocyte apoptosis inhibition

Cited by 88 publications

References 34 publications

Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury

Hypoxia-inducible factor-1 alpha is involved in RIP-induced necroptosis caused by in vitro and in vivo ischemic brain injury

Age-dependent modifications in vascular adhesion molecules and apoptosis after 48-h reperfusion in a rat global cerebral ischemia model

Puerarin Attenuates Osteoarthritis via Upregulating AMP-Activated Protein Kinase/Proliferator-Activated Receptor-γ Coactivator-1 Signaling Pathway in Osteoarthritis Rats

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