Cordycepin protects against β–amyloid and ibotenic acid– induced hippocampal CA1 pyramidal neuronal hyperactivity

Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.

Cordycepin protects against β–amyloid and ibotenic acid– induced hippocampal CA1 pyramidal neuronal hyperactivity

Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.

Cordycepin protects against β-amyloid and ibotenic acid-induced hippocampal CA1 pyramidal neuronal hyperactivity

Yao, Li-Hua,Wang, Jinxiu,Liu, Chao,Wei, Shanshan,Li, Guoyin,Wang, Songhua,Meng, Wei,Liu, Zhi-Bin,Huang, Li-Ping The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. ${\beta}$-Amyloid ($A{\beta}$) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in $A{\beta}$ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine $A_1$ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the $A{\beta}$ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of $A_1R$ is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.

Identification of differentially expressed miRNAs after Lactobacillus reuteri treatment in the ileum mucosa of piglets

Qi Wang,Qian Sun,Jing Wang,Xiaoyu Qiu,Renli Qi,Jinxiu Huang 한국유전학회 2020 Genes & Genomics Vol.42 No.11

Background Lactobacillus reuteri I5007 possesses many excellent probiotic characteristics in piglets. miRNA plays importantrole in host-microbiota interactions, but the mechanism by which L. reuteri I5007 regulates intestinal function throughits influence on miRNA expression is unknown. Objective This study analyzed the miRNA expression patterns in the ileum mucosa tissue of piglets by L. reuteri I5007treatment, aim to clarify its molecular mechanism for regulating intestinal function through miRNA. Methods Neonatal piglets were orally administered L. reuteri I5007 or a placebo daily starting on day 1, and differentialexpression of ileal miRNAs was analyzed at 10 and 20 days of age by small RNA sequencing. Results 361 known porcine miRNAs were identified, and ten miRNAs were highly expressed in the ileum mucosa in bothtreatments. Nineteen differentially expressed (DE) miRNAs were identified in response to L. reuteri treatment, and four DEmiRNAs (ssc-miR-196a, -196b-5p, -1285 and -10386) were differentially expressed at both time points. The KEGG pathwayanalyses showed the targets of 19 DE miRNAs were involved in 63 significantly enriched pathways, including the PI3KAktand MAPK pathways, which were confirmed to play important roles in probiotic-host communication. L. reuteri I5007exerted anti-inflammatory effects by influencing the levels of inflammatory cytokines. Suppressor of cytokine signalling 4gene was the target gene of ssc-miR-196a/-196b-5p, overexpression of ssc-miR-196a/-196b-5p downregulated the mRNAexpression of IL-1β and TNFα in IPEC-J2 cells. Conclusion Our study provides new insight into the role of miRNAs in the intestinal function of piglets after L. reuteriI5007 treatment.

Fabrication of Hollow Polymer Microchannels Using the MIMIC Technique with Subsequent Heat Treatment

Weiren Li,Wenqiang Xing,Fengzhou Zhao,Lichun Zhang,Yupeng Huang,Jinxiu Li,Linwei Zhu,Zheng Xu,Dengying Zhang 한국정밀공학회 2021 International Journal of Precision Engineering and Vol.22 No.8

The hollow polymer microchannels with different shapes and dimensions have been fabricated by the MIMIC method and the heating process for the first time. The smallest cross-sectional dimensions of hollow polymer microchannels were about 2.6 μm in the vertical direction and 3.5 μm in the horizontal direction. The length of hollow polymer microchannels increased parabolically with the heating temperature in the range of 30–135 °C. And the influence of the PDMS mold crosssectional areas on the length of the microchannels was invetigated. Furthermore, the forming mechanism of hollow polymer microchannels was disscussed in detail. This technique provides a cheap, simple and controllable way for the preparation of microchannels.