Combining Insulin-Like Growth Factor Derivatives Plus Caffeinol Produces Robust Neuroprotection After Stroke in Rats

Zhao, Xiurong; Liu, Shi Jie; Zhang, Jie; Strong, Roger; Aronowski, Jarek; Grotta, James C.

doi:10.1161/01.str.0000149624.87661.18

Cited by 33 publications

(29 citation statements)

References 30 publications

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“…Consistent with the present study Bickerdike and colleagues (2009) reported that continuous intravenous infusion of G-2MePE reduces the infarct size after endothelin1 (ET1) induced middle cerebral artery vasoconstriction in rats (Bickerdike et al , 2009). Zhao et al (2005) demonstrated that G-2MePE offers effective neuroprotection by reducing neuronal deficit scores at a 10 times lower dose compared to GPE, when treated in combination with caffeinol (Zhao et al , 2005).…”

Section: Discussionsupporting

confidence: 89%

Neuroprotection with Glycine-2-Methylproline-Glutamate (G-2MePE) after hypoxic-ischemic brain injury in adult rats

Mathai¹,

Harris²,

Brimble³

et al. 2014

J Exp Stroke Transl Med

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Background and Purpose: Hypoxic-ischemic brain injury, due to reduced supply of oxygen to brain, is a major cause of death and disability. There is no exclusive treatment available so far. Glycine-2-Methylproline-Glutamate (G-2MePE, NNZ 2566), an analogue of Glycine-Proline-Glutamate reduces neuronal injury after focal ischemia in adult rats. The current study investigated into the neuroprotective effects of G-2MePE after global hypoxic-ischemic brain injury in adult rats.Methods: Adult male rats received a single sub cutaneous injection of G-2MePE (1.2mg/kg) 3h post hypoxic-ischemic brain injury or the same volume of normal saline. Brains were extracted 5 days after the treatment. Tissue damage in the cortex, hippocampus and striatum was assessed. Neuronal survival, glial reactions, caspase-3 activity and TNF-α cytokine activity were also assessed.Results: The treatment with G-2MePE was associated with a significant reduction of tissue damage, improvement in neuronal survival, reduction in reactive microglia, TNF-α positive cells and caspase-3 positive cells in hippocampus and cortex but an elevation of astrocytosis.Conclusions: Neuroprotection with G-2MePE after hypoxic-ischemic brain injury in adult rats is associated with reduced neuronal necrosis, apoptosis, modulated inflammatory responses and augmented astrocytosis.

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Section: Discussionsupporting

confidence: 89%

Neuroprotection with Glycine-2-Methylproline-Glutamate (G-2MePE) after hypoxic-ischemic brain injury in adult rats

Mathai¹,

Harris²,

Brimble³

et al. 2014

J Exp Stroke Transl Med

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“…Adenosine, a ubiquitous neuromodulator, plays a key role in these changes by accumulating both during wakefulness and in response to ischemia, hypoxia, excitotoxicity, inflammation, and other types of TBI [31]. Interestingly, an agent that has significant effect on adenosine neurochemistry, caffeine, has also been demonstrated to exert neuroprotective effects after stroke [32] and other neurologic conditions [33][34]. The fact that one study found neuroprotective effects of caffeine when given chronically but not acutely [34] suggests that acute elevation of adenosine as seen with 24 h of SD may but protective, while longer duration SD may be detrimental to brain function.…”

Section: Discussionmentioning

confidence: 99%

Prior housing conditions and sleep loss may affect recovery from brain injury in rats: A pilot study

Riechers

Shuster²,

Bryan³

et al. 2013

JRRD

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Abstract-The purpose of this study is to understand the effect of combat-associated conditions such as sleep deprivation (SD) on subsequent traumatic brain injury (TBI). Prior to TBI (or sham surgery) induced by controlled cortical impact (CCI), rats were housed singly in chambers that prevented rapid eye movement sleep or allowed unrestricted sleep (no SD). Sensorimotor function was tested pre-SD and retested on postoperative days (PDs) 4, 7, and 14. Two additional control groups were housed socially prior to either CCI or sham surgery. CCI resulted in immediate performance deficits on sensorimotor tasks. The PD on which performance returned to baseline depended on preinjury conditions. Overall, preinjury SD+CCI resulted in an earlier recovery than no SD+CCI, and the no SD+CCI group (housed singly under conditions comparable with the SD group) recovered slower than all other groups. These data are the first to raise the possibility that recovery of sensorimotor function following TBI is affected by preinjury conditions. The data suggest that preinjury SD 24 h in duration may result in faster recovery and that novel or social isolation conditions may impede recovery. Thus, the combat environment may contribute to complexities associated with TBIs common in U.S. servicemembers.

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“…Another group studied the N-terminal tripeptide of IGF-1, Gly-Pro-Glu (GPE). 33 GPE (3 mg/kg/h), started 75 minutes after MCAO and continued for three days, improved the neurological disability score and reduced cortical infarct size by 45%. Studies on intranasally administered IGF-1 in stroke are described later in this review.…”

Section: Igf-1mentioning

confidence: 96%

Growth factors and stroke

Greenberg

Jin

2006

NeuroRX

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Summary: Current options for the treatment of stroke are extremely limited, partly because of the rapidity with which brain cells die when deprived of their blood supply. Several recent studies suggest that growth factors can produce improvement in animal models of stroke, even when administered at postischemic intervals of many hours to days, when conventional neuroprotective approaches are typically futile.Several growth factors can access the brain after systemic administration, making them more attractive as therapeutic agents. Finally, growth factors are key mediators of neurogenesis in the adult brain, which could have a role in brain repair and functional recovery following stroke.

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Combining Insulin-Like Growth Factor Derivatives Plus Caffeinol Produces Robust Neuroprotection After Stroke in Rats

Cited by 33 publications

References 30 publications

Neuroprotection with Glycine-2-Methylproline-Glutamate (G-2MePE) after hypoxic-ischemic brain injury in adult rats

Neuroprotection with Glycine-2-Methylproline-Glutamate (G-2MePE) after hypoxic-ischemic brain injury in adult rats

Prior housing conditions and sleep loss may affect recovery from brain injury in rats: A pilot study

Growth factors and stroke

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