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Poly-Arginine Peptide R18d Reduces Neuroinflammation And Functional Deficits Following Traumatic Brain Injury In The Long-Evans Rat, Li Shan Chiu, Ryan S. Anderton, Jane L. Cross, Vince W. Clark, Neville W. Knuckey, Bruno P. Meloni
Poly-Arginine Peptide R18d Reduces Neuroinflammation And Functional Deficits Following Traumatic Brain Injury In The Long-Evans Rat, Li Shan Chiu, Ryan S. Anderton, Jane L. Cross, Vince W. Clark, Neville W. Knuckey, Bruno P. Meloni
Health Sciences Papers and Journal Articles
We have previously demonstrated that the poly-arginine peptide R18 can improve histological and functional outcomes following traumatic brain injury (TBI) in the Sprague–Dawley rat. Since D-enantiomer peptides are often exploited in pharmacology for their increased stability and potency, the present study compared the effects of R18 and its D-enantiomer, R18D, following TBI in the Long-Evans rat. Following a closed-head impact delivered via a weight-drop apparatus, peptide was administered at a dose of 1000 nmol/kg at 30 min after TBI. Treatment with R18D, but not R18 resulted in significant reductions in sensorimotor (p = 0.026) and vestibulomotor (p = 0.049) deficits …
Proteomic Analysis Of Cortical Neuronal Cultures Treated With Poly-Arginine Peptide-18 (R18) And Exposed To Glutamic Acid Excitotoxicity, Gabriella Macdougall, Ryan S. Anderton, Frank L. Mastaglia, Neville W. Knuckey, Bruno P. Meloni
Proteomic Analysis Of Cortical Neuronal Cultures Treated With Poly-Arginine Peptide-18 (R18) And Exposed To Glutamic Acid Excitotoxicity, Gabriella Macdougall, Ryan S. Anderton, Frank L. Mastaglia, Neville W. Knuckey, Bruno P. Meloni
Health Sciences Papers and Journal Articles
Poly-arginine peptide-18 (R18) has recently emerged as a highly effective neuroprotective agent in experimental stroke models, and is particularly efficacious in protecting cortical neurons against glutamic acid excitotoxicity. While we have previously demonstrated that R18 can reduce excitotoxicity-induced neuronal calcium influx, other molecular events associated with R18 neuroprotection are yet to investigated. Therefore, in this study we were particularly interested in protein expression changes in R18 treated neurons subjected to excitotoxicity. Proteomic analysis was used to compare protein expression patterns in primary cortical neuronal cultures subjected to: (i) R18-treatment alone (R18); (ii) glutamic acid excitotoxic injury (Glut); (iii) R18-treatment and …
Poly-Arginine R18 And R18d (D-Enantiomer) Peptides Reduce Infarct Volume And Improves Behavioural Outcomes Following Perinatal Hypoxic-Ischaemic Encephalopathy In The P7 Rat, Adam B. Edwards, Jane L. Cross, Ryan S. Anderton, Neville W. Knuckey, Bruno P. Meloni
Poly-Arginine R18 And R18d (D-Enantiomer) Peptides Reduce Infarct Volume And Improves Behavioural Outcomes Following Perinatal Hypoxic-Ischaemic Encephalopathy In The P7 Rat, Adam B. Edwards, Jane L. Cross, Ryan S. Anderton, Neville W. Knuckey, Bruno P. Meloni
Health Sciences Papers and Journal Articles
We examined the neuroprotective efficacy of the poly-arginine peptide R18 and its D-enantiomer R18D in a perinatal hypoxic-ischaemic (HI) model in P7 Sprague-Dawley rats. R18 and R18D peptides were administered intraperitoneally at doses of 30, 100, 300 or 1000 nmol/kg immediately after HI (8% O2/92%N2 for 2.5 h). The previously characterised neuroprotective JNKI-1-TATD peptide at a dose of 1000 nmol/kg was used as a control. Infarct volume and behavioural outcomes were measured 48 h after HI. For the R18 and R18D doses examined, total infarct volume was reduced by 25.93% to 43.80% (P = 0.038 to < 0.001). By comparison, the JNKI-1-TATD reduced lesion volume by 25.27% (P = 0.073). Moreover, R18 and R18D treatment resulted in significant improvements in behavioural outcomes, while with JNKI-1-TATD there was a trend towards improvement. As an insight into the likely mechanism underlying the effects of R18, R18D and JNKI-1-TATD, the peptides were added to cortical neuronal cultures exposed to glutamic acid excitotoxicity, resulting in up to 89, 100 and 71% neuroprotection, respectively, and a dose dependent inhibition of neuronal calcium influx. The study further confirms the neuroprotective properties of polyarginine peptides, and suggests a potential therapeutic role for R18 and R18D in the treatment of HIE.
Perinatal Hypoxic-Ischemic Encephalopathy And Neuroprotective Peptide Therapies: A Case For Cationic Arginine-Rich Peptides (Carps), Adam B. Edwards, Ryan S. Anderton, Neville W. Knuckey, Bruno P. Meloni
Perinatal Hypoxic-Ischemic Encephalopathy And Neuroprotective Peptide Therapies: A Case For Cationic Arginine-Rich Peptides (Carps), Adam B. Edwards, Ryan S. Anderton, Neville W. Knuckey, Bruno P. Meloni
Health Sciences Papers and Journal Articles
Perinatal hypoxic-ischemic encephalopathy (HIE) is the leading cause of mortality and morbidity in neonates, with survivors suffering significant neurological sequelae including cerebral palsy, epilepsy, intellectual disability and autism spectrum disorders. While hypothermia is used clinically to reduce neurological injury following HIE, it is only used for term infants (>36 weeks gestation) in tertiary hospitals and improves outcomes in only 30% of patients. For these reasons, a more effective and easily administrable pharmacological therapeutic agent, that can be used in combination with hypothermia or alone when hypothermia cannot be applied, is urgently needed to treat pre-term (_36 weeks gestation) and …
Assessment Of R18, Cog1410, And App96-110 In Excitotoxicity And Traumatic Brain Injury, Li Shan Chiu, Ryan S. Anderton, Jane L. Cross, Vince W. Clark, Adam B. Edwards, Neville W. Knuckey, Bruno P. Meloni
Assessment Of R18, Cog1410, And App96-110 In Excitotoxicity And Traumatic Brain Injury, Li Shan Chiu, Ryan S. Anderton, Jane L. Cross, Vince W. Clark, Adam B. Edwards, Neville W. Knuckey, Bruno P. Meloni
Health Sciences Papers and Journal Articles
Cationic arginine-rich and poly-arginine peptides (referred to as CARPs) have potent neuroprotective properties in in vitro excitotoxicity and in vivo models of stroke. Traumatic brain injury (TBI) shares many pathophysiological processes as stroke, including excitotoxicity. Therefore, we evaluated our lead peptide, poly-arginine R18, with the COG1410 and APP96-110 peptides, which have neuroprotective actions following TBI. In an in vitro cortical neuronal glutamic acid excitotoxicity injury model, R18 was highly neuroprotective and reduced neuronal calcium influx, while COG1410 and APP96-110 displayed modest neuroprotection and were less effective at reducing calcium influx. In an impact-acceleration closed-head injury model (Marmarou model), R18, COG1410, …