Ischemic Reperfusion Injury in Rabbit Spinal Cord: Protective Effect of Superoxide Dismutase on Neurological Recovery and Spinal Infarction

1990 ◽  
Vol 137 (4) ◽  
pp. 303-310 ◽  
Author(s):  
Pedro Cuevas ◽  
Diana Reimers ◽  
Fernando Carceller ◽  
Araceli Jimenez
Keyword(s):  
Spinal Cord ◽  
Superoxide Dismutase ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Neurological Recovery ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

Adeno-associated virus packaged TRPC5 gene therapy alleviated spinal cord ischemic reperfusion injury in rats

Neuroreport ◽  
2020 ◽  
Vol 31 (1) ◽  
pp. 29-36
Author(s):  
Nana Shen ◽  
Lin Wang ◽  
Yiling Wu ◽  
Yanlin Liu ◽  
Haitao Pei ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Gene Therapy ◽  
Reperfusion Injury ◽  
Ischemic Reperfusion Injury ◽  
Adeno Associated Virus ◽  
Ischemic Reperfusion

scholarly journals Pengaruh Lidokain Intravena Terhadap Kadar Superoxide Dismutase 1 (Sod-1) Paru Kelinci Dengan Lung Ischemic Reperfusion Injury Model

2015 ◽  
Vol 7 (3) ◽  
pp. 146
Author(s):  
Mohammad Arief Kurniawan ◽  
Johan Arifin ◽  
Taufik Eko Nugroho
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Superoxide Dismutase 1 ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Injury Model

Latar belakang : Angka kejadian komplikasi paru paska operasi non jantung dibandingkan dengan komplikasi jantung yaitu 2,7% dan 2,5%. Penyebab hal ini adalah stres oksidatif, ketidakseimbangan radikal oksigen dan endogenous scavenging system.Lidokain  menghambat saluran natrium dan, mengurangi masukan kalsium intraseluler, mengurangi produksi Reactive Oxygen Species (ROS) dan modulasi bioenergetika mitokondria, sehingga diharapkan lidokain mampu meningkatkan kadar antioksidan alami di dalam sel.Superoxide Dismutase-1 (SOD-1) adalah salah satu antioksidan alami didalam sel yang berperan dalam melindungi organ dari anion superoksida yang berbahaya dengan mengubah anion yang dihasilkan dari cedera setelah ischaemia-reperfusion.Tujuan : Mengetahui efek lidokain intravena terhadap kadar Superoxide Dismutase 1 (SOD-1) paru kelinci dengan lung ischemic reperfusion injury model.Metode : Desain eksperimental laboratorik, 16 kelinci dibagi menjadi dua kelompok secara acak. Kelompok kontrol mendapat perlakuan lung ischemic reperfusion injury dan kelompok perlakuan dilakukan lung ischemic reperfusion injurydan mendapat injeksi lidokain 1,5mg/kgBB/jam intravena secara kontinyu kemudian diukur kadar SOD-1 jaringan paru kedua kelompok. Uji normalitas menggunakan uji Shapiro Wilk dilanjutkan uji beda Independent T-test.Hasil : Kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injurydan mendapat lidokain lebih tinggi secara signifikan (p=0,01) dibandingkan dengan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injuryKesimpulan : Pemberian lidokain kontinyu intravena dapat meningkatkan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injury. 

scholarly journals Protective Effect of Pharmacological Preconditioning of Total Flavones of Abelmoschl Manihot on Cerebral Ischemic Reperfusion Injury in Rats

2007 ◽  
Vol 35 (04) ◽  
pp. 653-661 ◽  
Author(s):  
Ji-Yue Wen ◽  
Zhi-Wu Chen
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inos Mrna ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Infarction Volume ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
Pharmacological Preconditioning

The present study was to investigate the effect of pharmacological preconditioning of total flavones of Abelmoschl Manihot (TFA) on cerebral ischemic reperfusion injury in rats. Rat cerebral ischemia/reperfusion injury was induced by occluding the right middle cerebral artery (MCA). The infarct size was determined by staining with 2,3,5-triphenyl tetrazalium chloride (TTC). The serum malonaldehyde (MDA), nitric oxide (NO) and lactate dehydrogenase (LDH) levels were measured by using spectrophotometry; Inducible NO synthase (iNOS) mRNA expression was detected by RT-PCR method. The percentage of cerebral infarction volume was 28.1 ± 0.8 in the model group, while TFA or nimodipine (Nim) pretreatment 36 hours prior to the ischemic insult significantly decreased the infarction volume. Increases of serum LDH activity and MDA level were observed after ischemia/reperfusion, but these changes were inhibited in rats pretreated with either TFA (20, 40, 80, 160 mg/kg) or Nim, indicating a delayed protective effect of TFA preconditioning on cerebral ischemic reperfusion injury. In addition, the serum NO level and the cerebral iNOS mRNA were up-regulated, suggesting a possible mechanism for the protective effect of TFA pretreatment on cerebral ischemic reperfusion injury.

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