Neuroprotection of a Novel Synthetic Caffeic Acid-Syringic Acid Hybrid Compound against Experimentally Induced Transient Cerebral Ischemic Damage

Kim, In Hye; Yan, Bing Chun; Park, Joon Ha; Yeun, Go Heum; Yim, Yongbae; Ahn, Ji Hyeon; Lee, Jae Chul; Hwang, In Koo; Cho, Jun Hwi; Kim, Young‐Myeong; Lee, Yun Lyul; Park, Jeong Ho; Won, Moo‐Ho

doi:10.1055/s-0032-1328211

Cited by 26 publications

(15 citation statements)

References 37 publications

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“…We found a significant loss of pyramidal neurons in stratum pyramidale of the ischemic CA1 region in the ischemia-groups 5 days after ischemia-reperfusion using NeuN immunohistochemistry and F-J B histofluorescence staining. This outcome is consistent with our previous studies using the same animal model [21,29,30].…”

Section: Discussionsupporting

confidence: 93%

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

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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.

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Section: Discussionsupporting

confidence: 93%

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

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“…10 Kim et al found that a caffeic acid-syringic acid hybrid compound showed a strong neuroprotective effect in transient cerebral ischemia. 29 Although Kumar et al 24 showed that SA administration preserves the functional capacity of the kidney from adverse effects in hypertensive rats, there was no study showing the effect of SA on renal IR found in our review of the literature. Itoh et al reported that SA significantly suppressed the increase in inflammatory cytokines TNF-a, IFN-g and IL-6; and the suppressive effect of SA on Concanavalin Ainduced liver injury might be due to scavenging of ROS generated by activated NADPH oxidase in the lymphocytes.…”

Section: Discussionmentioning

confidence: 73%

“…28 In recent years, serum lipid peroxidation activities have been analyzed by evaluating the TOS. 29 The protecting enzymes, SOD, CAT and GPx, react against the devastating actions of ROS and these molecules comprise the TAS. The advantage of TAS measurement is that it measures the antioxidant capacity of all antioxidants in a biological sample.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of syringic acid on kidney ischemia-reperfusion injury

et al. 2016

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“…Transient cerebral ischemia was developed following our previous method (Kim et al, 2013). The experimental animals were anesthetized with a mixture of 2.5% isoflurane in 33% oxygen and 67% nitrous oxide.…”

Section: Induction Of Transient Cerebral Ischemiamentioning

confidence: 99%

Comparison of neuroprotective effects of extract and fractions fromAgarum clathratumagainst experimentally induced transient cerebral ischemic damage

Kim

Yoo

Park

et al. 2013

Pharmaceutical Biology

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Objective: We investigated the neuroprotective effects of crude-extract, ethyl acetate (EA)-, n-butanol (BU)-, dichloromethane (DCM)-and n-hexane (Hx)-fractions from A. clathratum on ischemic damage in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. Materials and methods: Agarum clathratum was collected in Kangwon province (South Korea) and treated with 95% ethanol. The ethanol extract was suspended in distilled water and subjected to a series of partitions with EA, BU, DCM and Hx. Each of extract and fraction was orally administered with 50 mg/kg once a day for one week before ischemia-reperfusion (I-R).Result: In the crude-extract-, EA-and BU-fraction-treated ischemia groups, we found strong neuroprotection in the CA1 -about 80-89% of CA1 pyramidal neurons survived. However, in the DCM-and Hx-fraction-treated ischemia groups, we did not find any significant neuroprotection. In addition, we observed changes in astrocytes and microglia in the ischemic CA1. In the crude-extract, EA-and BU-fraction-treated ischemia groups, the distribution pattern and activity of the glial cells were similar to that found in the sham group. Discussion: Repeated supplements of crude-extract, EA-and BU-fractions of A. clathratum could protect neurons from I-R injury in the hippocampal CA1 induced by transient cerebral ischemia via decrease of glial activation.

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Neuroprotection of a Novel Synthetic Caffeic Acid-Syringic Acid Hybrid Compound against Experimentally Induced Transient Cerebral Ischemic Damage

Cited by 26 publications

References 37 publications

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

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

Protective effect of syringic acid on kidney ischemia-reperfusion injury

Comparison of neuroprotective effects of extract and fractions fromAgarum clathratumagainst experimentally induced transient cerebral ischemic damage

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