Maintenance of anti-inflammatory cytokines and reduction of glial activation in the ischemic hippocampal CA1 region preconditioned with lipopolysaccharide

Yu, Jia Tian; Lee, Choong Hyun; Yoo, Ki‐Yeon; Choi, Jung Hoon; Li, Hua; Park, Ok Kyu; Yan, Bingchun; Hwang, In Koo; Kwon, Young Guen; Kim, Young Myeong; Won, Moo Ho

doi:10.1016/j.jns.2010.06.004

Cited by 51 publications

(32 citation statements)

References 48 publications

(53 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NeuN immunohistochemistry and Fluoro-Jade B (F-J B) histofluorescence staining were done according to the methods of the previous studies [24]. In brief, the sections were sequentially treated with 0.3 % hydrogen peroxide in PBS for 30 min and 10 % normal goat serum in 0.05 M PBS for 30 min.…”

Section: Neun Immunohistochemistry and F-j B Stainingmentioning

confidence: 99%

“…To confirm changes in protein levels in the CA1 following transient cerebral ischemia, animals (n = 5 in each group) were sacrificed and used for western blot analysis at designed times after IR according to the method of our previous study [24]. In brief, after sacrificing them and removing the brain, it was serially and transversely cut into a thickness of 400-lm on a vibratome (Leica), and the hippocampal CA1 region was then dissected with a surgical blade.…”

Section: Neun Immunohistochemistry and F-j B Stainingmentioning

confidence: 99%

See 1 more Smart Citation

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

et al. 2014

Self Cite

View full text Add to dashboard Cite

In this study, we investigated the effects of a normal diet (ND) and high-fat diet (HFD) on delayed neuronal death in the gerbil hippocampal CA1 region after transient cerebral ischemia. In the HFD-fed gerbils, ischemia-induced hyperactivity was significantly increased and neuronal damage was represented more severely compared to the ND-fed gerbils. Ischemia-induced glial activation was accelerated in the HFD-fed gerbils. Cytokines including interleukin-2 and -4 were more sensitive in the hippocampal CA1 region of the HFD-fed gerbils after ischemia-reperfusion. Additionally, we found that decreased 4-HNE and SODs immunoreactivity and protein levels in the hippocampal CA1 region of the HFD-fed gerbils after ischemia-reperfusion. These results indicate that HFD may lead to the exacerbated effects on ischemia-induced neuronal death in the hippocampal CA1 region after ischemia-reperfusion. These effects of HFD may be associated with more accelerated activations of glial cells and imbalance of pro- and anti-inflammatory cytokines and/or antioxidants after transient cerebral ischemia.

show abstract

Section: Neun Immunohistochemistry and F-j B Stainingmentioning

confidence: 99%

Section: Neun Immunohistochemistry and F-j B Stainingmentioning

confidence: 99%

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…To examine the neuronal death in the hippocampus after repeated restraint stress, NeuN immunohistochemistry and Fluoro-Jade B (F-J B) histofluorescence staining were done according to the methods of the previous studies [24,25]. In brief, the sections were sequentially treated with 0.3% hydrogen peroxide (H2O2) in PBS for 30 min and 10% normal goat serum in 0.05 M PBS for 30 min.…”

Section: Staining For Neuronal Damagementioning

confidence: 99%

“…The effect of chronic restraint stress on the changes in GR and Iba-1 immunoreactivity was examined according to the previous method [25,26]. Semi-quantification of immunostaining intensities for GR was evaluated with digital image analysis software (MetaMorph 4.01, Universal Imaging Corp.).…”

Section: Staining For Neuronal Damagementioning

confidence: 99%

Comparison of Glucocorticoid Receptor and Ionized Calcium-Binding Adapter Molecule 1 Immunoreactivity in the Adult and Aged Gerbil Hippocampus Following Repeated Restraint Stress

et al. 2011

Self Cite

View full text Add to dashboard Cite

Stress leads to changes in homeostasis and internal balance of the body and is known to be one of important factors in the development of several diseases. In the present study, we investigated changes in glucocorticoid receptor (GR) and ionized calcium-binding adapter molecule 1 (Iba-1) immunoreactivity in the adult and aged gerbil hippocampus after chronic restraint stress. Serum corticosterone level was much higher in both the stress-groups than the control groups. No neuronal death was found in all hippocampal subregions of the adult and aged gerbil after chronic restraint stress. GR immunoreactivity was decreased in both the adult and aged groups after repeated restraint stress; however, GR immunoreactivity in the adult-stress-group was decreased much more than that in the aged-stress-group. Iba-1 immunoreactive microglia were hypertrophied and activated in the adult group after repeated restraint stress; in the aged-stress-group, there was no any significant change in Iba-1 immunoreactive microglia. In brief, level of GR, not Iba-1, in the hippocampus was much decreased in the adult gerbil compared to the aged gerbil following chronic restraint stress.

show abstract

“…The brain induced by IPC shows neuroprotection in the hippocampal CA1 region, and we surmise a steady expression of anti-inflammatory cytokines which are related to the resolution of brain inflammation; anti-inflammatory cytokines including IL-4 and IL-13 might be involved in the resolution of brain inflammation [17,18]. Cellular inflammatory responses display important roles in ischemic injury and anti-inflammatory treatments in ischemic stroke must be beneficial [19].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

et al. 2015

Self Cite

View full text Add to dashboard Cite

Ischemic preconditioning (IPC) induced by sublethal transient cerebral ischemia could reduce neuronal damage/death following a subsequent lethal transient cerebral ischemia. We, in this study, compared expressions of interleukin (IL)-2 and tumor necrosis factor (TNF)-α as pro-inflammatory cytokines, and IL-4 and IL-13 as anti-inflammatory cytokines in the gerbil hippocampal CA1 region between animals with lethal ischemia and ones with IPC followed by lethal ischemia. In the animals with lethal ischemia, pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region were dead at 5 days post-ischemia; however, IPC protected the CA1 pyramidal neurons from lethal ischemic injury. Expressions of all cytokines were significantly decreased in the SP after lethal ischemia and hardly detected in the SP at 5 days post-ischemia because the CA1 pyramidal neurons were dead. IPC increased expressions of anti-inflammatory cytokines (IL-4 and IL-13) in the stratum pyramidale of the CA1 region following no lethal ischemia (sham-operation), and the increased expressions of IL-4 and IL-13 by IPC were continuously maintained is the SP of the CA1 region after lethal ischemia. However, pro-inflammatory cytokines (IL-2 and TNF-α) in the SP of the CA1 region were similar those in the sham-operated animals with IPC, and the IL-4 and IL-13 expressions in the SP were maintained after lethal ischemia. In conclusion, this study shows that anti-inflammatory cytokines significantly increased and longer maintained by IPC and this might be closely associated with neuroprotection after lethal transient cerebral ischemia.

show abstract

Maintenance of anti-inflammatory cytokines and reduction of glial activation in the ischemic hippocampal CA1 region preconditioned with lipopolysaccharide

Cited by 51 publications

References 48 publications

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

Comparison of Glucocorticoid Receptor and Ionized Calcium-Binding Adapter Molecule 1 Immunoreactivity in the Adult and Aged Gerbil Hippocampus Following Repeated Restraint Stress

Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

Contact Info

Product

Resources

About