H290-51

01/01/1997 - "This compound (H-290/51) has neuro-protective effects on edema and cell changes in this model. "
01/01/2023 - "Our results show that nanodelivery of H-290/51 with MSCs significantly enhanced CBF and reduced BBB breakdown, edema formation and brain pathology following METH exposure at hot environment. "
03/15/1997 - "Pretreatment with H-290/51 significantly attenuated the upregulation of c-NOS in animals subjected to HS, and the signs of neuronal distortion and edema were less pronounced. "
01/01/2003 - "Pre-treatment with H-290/51 markedly attenuated the trauma-induced cNOS and iNOS expression along with the microvascular permeability disturbances, edema formation and cell injury. "
01/01/2000 - "Pretreatment with H-290/51 (50 mg/kg, p.o., 30 min before trauma) significantly attenuated the HO-2 immunoreactivity along with breakdown of the BSCB permeability, edema and cell injury. "

01/01/2003 - "Pre-treatment with H-290/51 markedly attenuated the trauma-induced cNOS and iNOS expression along with the microvascular permeability disturbances, edema formation and cell injury. "
01/01/2000 - "Pretreatment with H-290/51 (50 mg/kg, p.o., 30 min before trauma) significantly attenuated the HO-2 immunoreactivity along with breakdown of the BSCB permeability, edema and cell injury. "
04/01/2006 - "Taken together, these observations suggest that (i) oxidative stress participates in HSP response following trauma, and (ii) the antioxidant compound H-290/51 attenuates cellularstress, improves motor functions and induces considerable neuroprotection in the early phase of SCI. Further studies using post-injury treatment with H-290/51 is needed to explore its therapeutic potentials in clinical settings."
01/01/1997 - "The results indicate that a focal trauma induces widespread alterations in spinal cord SPE activity which can be influenced by the anti-oxidant drug H 290/51, suggesting that SPE is somehow involved in cell injury."
01/01/2002 - "Pretreatment with H-290/51 (50 mg/kg, p.o.), a potent antioxidant compound, effectively reduced the blood-spinal cord barrier (BSCB) permeability, edema formation and cell injury following trauma. "

01/01/2023 - "These observations suggests that histamine receptors are involved in the pathophysiology of spinal cord injury and induce superior neuroprotection in combination with an inhibitor of lipid peroxidation H-290/51, not reported earlier. "
01/01/2002 - "the antioxidant compound H-290/51 has a potential therapeutic value in the treatment of spinal cord injuries."
01/01/2000 - "Furthermore, our observations indicate that oxidative stress is involved in CO production, as reflected by HO-2 expression, which is injurious to the cord and H-290/51 exerts powerful neuroprotective effects in spinal cord injury."
01/01/2006 - "Post-injury treatment with a new antioxidant compound H-290/51 attenuates spinal cord trauma-induced c-fos expression, motor dysfunction, edema formation, and cell injury in the rat."
01/01/2023 - "In this investigation we used a combination of histaminergic drugs with antioxidant compound H-290/51 using their nanowired delivery for neuroprotection in spinal cord injury of longer duration. "

01/01/1998 - "Our results suggest that hyperthermic brain injury is associated with a marked upregulation of NOS activity in the CNS and this upregulation of NOS and concomitant cell injury can be reduced by prior treatment with an antioxidant compound H 290/51. "
03/15/1997 - "These results suggest that HS has the capacity to induce upregulation of c-NOS, and these effects can be reduced by prior treatment with H-290/51, indicating a possible neuroprotective effect of antioxidants in thermal brain injury."
01/01/2000 - "A new antioxidant compound H-290/51 attenuates nitric oxide synthase and heme oxygenase expression following hyperthermic brain injury. "

01/01/2010 - "Our results show that H-290/51 significantly attenuated heat stress induced BBB impairment, brain edema formation and neurotoxicity in nanoparticle treated rats. "
01/01/2010 - "Pretreatment with an antioxidant H-290/51 markedly attenuated the BBB dysfunction, brain edema formation and brain pathology during morphine withdrawal phases. "