Effects of L-Tetrahydropalmatine on neuron apoptosis during acute cerebral ischemia-reperfusion of rats

2000 ◽  
Vol 20 (2) ◽  
pp. 106-108 ◽  
Author(s):  
Yang Guangtian ◽  
Jiang Chonghui ◽  
Tang Yan ◽  
Wang Peihua
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Acute Cerebral Ischemia ◽  
Neuron Apoptosis

scholarly journals Preconditioning with L-alanyl-L-glutamine in a Mongolian Gerbil model of acute cerebral ischemia/reperfusion injury

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 14-20 ◽  
Author(s):  
Vilma Leite de Sousa Pires ◽  
José Reniclebson Feitosa de Souza ◽  
Sergio Botelho Guimarães ◽  
Antonio Ribeiro da Silva Filho ◽  
José Huygens Parente Garcia ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Femoral Vein ◽  
Control Group ◽  
Mongolian Gerbils ◽  
Cerebral Tissue ◽  
Arterial Blood ◽  
Cerebral Ischemia Reperfusion ◽  
Acute Cerebral Ischemia

PURPOSE: To investigate the effect of L-alanyl-L-glutamine (L-Ala-Gln) preconditioning in an acute cerebral ischemia/reperfusion (I/R) model in gerbils. METHODS: Thirty-six Mongolian gerbils (Meriones unguiculatus), (60-100g), were randomized in 2 groups (n=18) and preconditioned with saline 2.0 ml (Group-S) or 0.75g/Kg of L-Ala-Gln, (Group-G) administered into the femoral vein 30 minutes prior to I/R. Each group was divided into three subgroups (n=6). Anesthetized animals (urethane, 1.5g/Kg, i.p.) were submitted to bilateral occlusion of common carotid arteries during 15 minutes. Samples (brain tissue and arterial blood) were collected at the end of ischemia (T0) and after 30 (T30) and 60 minutes (T60) for glucose, lactate, myeloperoxidase (MPO), thiobarbituric acid reactive substances (TBARS), glutathione (GSH) assays and histopathological evaluation. RESULTS: Glucose and lactate levels were not different in studied groups. However glycemia increased significantly in saline groups at the end of the reperfusion period. TBARS levels were significantly different, comparing treated (Group-G) and control group after 30 minutes of reperfusion (p<0.05) in cerebral tissue. Pretreatment with L-Ala-Gln promoted a significant increase in cerebral GSH contents in Group-G at T30 (p<0.001) time-point compared with Group-S. At T30 and T60, increased levels of GSH occurred in both time-points. There were no group differences regarding MPO levels. Pyknosis, presence of red neurons and intracellular edema were significantly smaller in Group-G. CONCLUSION: Preconditioning with L-Ala-Gln in gerbils submitted to cerebral ischemia/reperfusion reduces oxidative stress and degeneration of the nucleus (pyknosis) and cell death (red neurons) in the cerebral tissue.

Combined bone marrow stromal cells and oxiracetam treatments ameliorates acute cerebral ischemia/reperfusion injury through TRPC6

2019 ◽  
Vol 51 (8) ◽  
pp. 767-777 ◽  
Author(s):  
Jing Wang ◽  
Ruohan Sun ◽  
Zhenzhu Li ◽  
Yujun Pan
Keyword(s):  
Bone Marrow ◽  
Cerebral Ischemia ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Ischemia Reperfusion ◽  
Marrow Stromal Cells ◽  
Neuron Survival ◽  
Cerebral Ischemia Reperfusion ◽  
Survival Pathway ◽  
Acute Cerebral Ischemia

Abstract Ischemic stroke has become one of the leading causes of deaths and disabilities all over the world. In this study, we investigated the therapeutic effects of combined bone marrow stromal cells (BMSCs) and oxiracetam treatments on acute cerebral ischemia/reperfusion (I/R) injury. A rat model of middle cerebral artery occlusion (MCAO) followed by complete reperfusion, as well as a cortex neuron oxygen-glucose deprivation (OGD) model was established. When compared with BMSCs or oxiracetam monotherapy, combination therapy significantly improved functional restoration with decreased infarct volume in observed ischemic brain. We propose that it may occur through the transient receptor potential canonical (TRPC)6 neuron survival pathway. The increased expression of TRPC6 along with the reduction of neuronal cell death in the OGD cortex neurons and combination therapy group indicated that the TRPC6 neuron survival pathway plays an important role in the combined BMSCs and oxiracetam treatments. We further tested the activity of the calpain proteolytic system, and the results suggested that oxiracetam could protect the integrity of TRPC6 neuron survival pathway by inhibiting TRPC6 degradation. The protein levels of phospho-cAMP response element binding protein (p-CREB) were tested. It was found that BMSCs play a role in the activation of the TRPC6 pathway. Our study suggests that the TRPC6 neuron survival pathway plays a significant role in the protective effect of combined BMSCs and oxiracetam treatments on acute cerebral I/R injury. Combined therapy could inhibit the abnormal degradation of TRPC6 via decreasing the activity of calpain and increasing the activation of TRPC6 neuron survival pathway.

scholarly journals TAK-242, an Antagonist for Toll-like Receptor 4, Protects against Acute Cerebral Ischemia/Reperfusion Injury in Mice

2015 ◽  
Vol 35 (4) ◽  
pp. 536-542 ◽  
Author(s):  
Fang Hua ◽  
Huiling Tang ◽  
Jun Wang ◽  
Megan C Prunty ◽  
Xiaodong Hua ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Inflammatory Cytokines ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling ◽  
Cerebral Ischemia Reperfusion ◽  
Acute Cerebral Ischemia

Toll-like receptor 4 (TLR4) contributes to cerebral ischemia/reperfusion (I/R) injury and is a potential target for the treatment of ischemic stroke. This experiment is to evaluate the effect of an exogenous TLR4 antagonist, TAK-242, against acute cerebral I/R injury. A mouse model of cerebral I/R was induced by transient middle cerebral artery occlusion. TAK-242 (3 mg/kg body weight) was injected intraperitoneally 1 hour after ischemia. Our results showed that the concentration of TAK-242 in plasma increased to 52.0 ng/mL 3 hours after injection, was maintained at 54.1 ng/mL 8 hours after injection, and decreased to 22.6 ng/mL 24 hours after injection. The concentration of TAK-242 in brain tissue increased to 26.1 ng/mL in ischemic hemisphere and 14.2 ng/mL in nonischemic hemisphere 3 hours after injection, and was maintained at the similar levels 24 hours after injection. We found that TAK-242 significantly reduced cerebral infarction compared with vehicle control, improved neurologic function, inhibited the phosphorylation of downstream protein kinases in TLR4 signaling pathway, and downregulated the expression of inflammatory cytokines. We conclude that TAK-242 is able to cross blood-brain barrier, blocks TLR4 signaling, mediates the expression of inflammatory cytokines, and protects the brain from acute damage induced by I/R.

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