The effect of biodegradable gelatin microspheres on the neuroprotective effects of high mobility group box 1 A box in the postischemic brain

Jin, Yin Chuan; Kim, Seung-Woo; Cheng, Felice; Shin, Jong-Gye; Park, Jin Kuen; Lee, Sang‐Hyun; Lee, Jung Eun; Han, Pyung Lim; Lee, Minhyung; Kim, Kyekyoon Kevin; Choi, Hyungsoo; Lee, Ja Kyeong

doi:10.1016/j.biomaterials.2010.09.054

Cited by 35 publications

(12 citation statements)

References 37 publications

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“…We have reported that SNMC, a glycyrrhizin-containing preparation developed for chronic liver disease, has a marked neuroprotective function in the postischemic brain via its anti-inflammatory effects [32] and SNMC shows significantly higher neuroprotective potency compared to an equivalent dose of pure glycyrrhizin, in terms of reducing infarct volume and improving neurological deficits [32]. Considering robust neuroprotective effects of GL in KA-induced animal seizure model in the present study and in MCAO animal model in our previous reports, investigation on the improvement of therapeutic potency of GL by modification and by producing formulation is worth pursuing.…”

Section: Discussionmentioning

confidence: 99%

Glycyrrhizin Attenuates Kainic Acid-Induced Neuronal Cell Death in the Mouse Hippocampus

et al. 2013

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Glycyrrhizin (GL), a triterpene that is present in the roots and rhizomes of licorice (Glycyrrhiza glabra), has been reported to have anti-inflammatory and anti-viral effects. Recently, we demonstrated that GL produced the neuroprotective effects with the suppression of microglia activation and proinflammatory cytokine induction in the postischemic brain with middle cerebral artery occlusion (MCAO) in rats and improved motor impairment and neurological deficits. In the present study, we investigated whether GL has a beneficial effect in kainic acid (KA)-induced neuronal death model. Intracerebroventricular (i.c.v.) injection of 0.94 nmole (0.2 µg) of KA produced typical neuronal death in both CA1 and CA3 regions of the hippocampus. In contrast, administration of GL (10 mg/kg, i.p.) 30 min before KA administration significantly suppressed the neuronal death, and this protective effect was more stronger at 50 mg/kg. Moreover, the GL-mediated neuroprotection was accompanied with the suppression of gliosis and induction of proinflammatory markers (COX-2, iNOS, and TNF-α). The anti-inflammatory and anti-excitotoxic effects of GL were verified in LPS-treated primary microglial cultures and in NMDA- or KA-treated primary cortical cultures. Together these results suggest that GL confers the neuroprotection through the mechanism of anti-inflammatory and anti-excitotoxic effects in KA-treated brain.

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Section: Discussionmentioning

confidence: 99%

Glycyrrhizin Attenuates Kainic Acid-Induced Neuronal Cell Death in the Mouse Hippocampus

et al. 2013

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“…It is well established that HMGB1-mediated inflammation may be a cause of cerebral I/R-induced brain damage (16). Previous research has demonstrated that inhibition of HMGB1 is associated with suppression of infarct formation (17,18). Other studies have implied that NF-κB may be a key regulator of inflammation during and subsequent to brain damage (19,20).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb1 administration attenuates focal cerebral ischemic reperfusion injury through inhibition of HMGB1 and inflammation signals

et al. 2018

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High-mobility group box 1 (HMGB1) is released after focal cerebral ischemia/reperfusion (I/R), and aggravates brain tissue damage. Ginsenoside Rb1 (Rb1), isolated from Panax ginseng, has been reported to inhibit I/R-induced cell death in the brain. The present study aimed to investigate the protective ability of GRb1 on focal cerebral I/R rats and to explore its further mechanisms. A middle cerebral artery occlusion (MCAO) rat model was established and treated with different doses of Rb1. The neurological deficits were examined after reperfusion, and TTC staining was applied to assess the infarct volume. Histology and TUNEL staining were performed to evaluate pathological changes and neuronal cell apoptosis in brain tissues. HMGB1 and levels of inflammatory factors and proteins, were examined by ELISA or western blotting. Rb1 treatment notably improved the neurological deficits in an MCAO model, accompanied by decreased infarct volume in the brain tissues. Histological examination revealed that the necrotic tissue area in MCAO rats was also diminished by Rb1 treatment. Apoptosis induced by cerebral I/R was also attenuated by Rb1 treatment via downregulation of cleaved caspase-3 and caspase-9 levels. HMGB1 release was inhibited by Rb1 treatment in MCAO rats, and the levels of nuclear factor-κB, tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase and nitric oxide were also decreased. The present study suggests that Rb1 serves a protective role in I/R-induced cerebral-neuron injury, due to the decreased cerebral infarct volume of brain tissue. The mechanisms underlying these effects may be associated with the inhibition of HMGB1 inflammatory signals.

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“…However, potential adverse ill-effects on cardiac function through its NMDA-antagonism, induction of psychotic-like symptoms, as well as the causation of selective neurotoxicity in brain regions outside the infarct area (so-called lesions of Olney) have thus far prevented its clinical translation [8]. For instance, high mobility group box one (HMGB1) A box released from gelatin microspheres injected into stroke-induced brain damage has been shown to attenuate the formation of proinflammatory cytokines, resulting in a decrease in infarct volume and improved neurological outcomes [10]. Moreover, larger molecules can be delivered that typically would not cross the blood-brain barrier [9].…”

Section: Introductionmentioning

confidence: 99%

Bioengineering solutions for neural repair and recovery in stroke

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Ambrosio²,

Friedlander³

et al. 2013

Current Opinion in Neurology

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The effect of biodegradable gelatin microspheres on the neuroprotective effects of high mobility group box 1 A box in the postischemic brain

Cited by 35 publications

References 37 publications

Glycyrrhizin Attenuates Kainic Acid-Induced Neuronal Cell Death in the Mouse Hippocampus

Glycyrrhizin Attenuates Kainic Acid-Induced Neuronal Cell Death in the Mouse Hippocampus

Ginsenoside Rb1 administration attenuates focal cerebral ischemic reperfusion injury through inhibition of HMGB1 and inflammation signals

Bioengineering solutions for neural repair and recovery in stroke

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