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38. Neuroprotective Effects of High-Intensity Interval Training through Neuroplastic Changes in a Restraint Stress-Induced Depression Model.

Author

Hwang, Dong-Joo, Um, Hyun-Seob, Choi, Dong-Hun, and Cho, Joon-Yong

Subjects
HIGH-intensity interval training, GLIAL fibrillary acidic protein, BRAIN-derived neurotrophic factor, IMMOBILIZATION stress
Abstract

This study aimed to analyze the neuroprotective effects of various exercise intensities in a mouse model of depressive behavior disorders. Seven-week-old male C57BL/6 mice were divided into a control group, depressive disorder group (RST), moderate-intensity sustained exercise group (RST_MICT), high-intensity sustained exercise group (RST_HICT), and high-intensity interval exercise group (RST_HIIT). The animal model was established by applying restraint stress (RST) at 2 h/day for 14 days. Behavioral function was better in all exercise groups, especially in the RST_HIIT group, than in the RST group. Factors related to brain-derived neurotrophic factor showed higher levels in the exercise groups than in the RST group. The levels of 4-hydroxynonenal, an oxidative stress index, were significantly lower in the exercise groups than in the RST group. Malondialdehyde levels were lower in the exercise groups than in the RST group, but the difference was not significant. The analysis of serotonin and corticosterone, indicators of depression, revealed positive results in the exercise groups. The neuroplasticity-related variables c-fos and glial fibrillary acidic protein were more positive in the RST_HIIT group than in the RST group. Thus, HIIT improved neuroplasticity, oxidative stress, and neurotrophic factors in the depressive disorder model, indicating its potential for preventing and treating depression. [ABSTRACT FROM AUTHOR]

Published
2023
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48. The Effects of 12 Weeks Pilates Mat Exercise on Body Composition, Lumbar Muscle Strength, Low Back Pain and Pregnancy Stress in Pregnant Women

Author

Cho Na Yung, Cho Joon Yong, and Yongchul Jang

Subjects
Pregnancy, medicine.medical_specialty, Lumbar, business.industry, Internal medicine, medicine, Muscle strength, medicine.symptom, medicine.disease, business, Low back pain, Gastroenterology
Abstract

임신 기간 중 임산부는 체중 증가 및 근골격계 변화로 요통과 골반 통증을 유발한다. 필라테스는 유, 무산소성 복합운동으로 자세 교정 및 근 기능을 강화시키는 것으로 보고되고 있다. 따라서 이 연구는 필라테스 매트 운동이 임산부의 신체구성, 요부근력, 요통 및 임신 스트레스에 미치는 영향을 규명하는데 목적이 있다. 본 연구를 수행하기 위해 임신 중기(16~25주) 임산부 19명을 대상으로 필라테스 매트 운동 실험집단(n=11)과 비교집단(n=8)으로 구분하였으며, 실험집단은 하루 60분, 주 2회 12주간 필라테스 매트 운동을 실시하였다. 신체구성 중 체수분량, 체지방량, 체질량지수, 체지방률 및 기초대사량에는 집단 간 변화가 없는 것으로 나타난 반면 실험집단에서는 골격근량에서 유의한 증가가 나타났다. 또한 요부근력의 경우 엉덩이관절 신전근과 요추 신전 가동범위는 필라테스 매트 운동을 수행한 집단에서 유의하게 증가하였다. 요통 수준과 임신 스트레스 수준을 분석한 결과 집단 간 차이는 없는 것으로 나타났다. 따라서 필라테스 매트 운동은 임산부의 근육량을 증가시키고, 요부근력에는 긍정적인 영향을 나타내어 임산부에게 안전하게 적용할 수 있는 운동이라고 할 수 있다.

Published
2020

50. Additional file 1 of Phosphodiesterase 5 inhibitor mirodenafil ameliorates Alzheimer-like pathology and symptoms by multimodal actions

Author

Kang, Byung Woo, Kim, Fred, Cho, Joon-Yong, Kim, SangYun, Rhee, Jinseol, and Choung, Jai Jun

Abstract

Additional file 1: Tables S1-S3. Figure S1. Semiquantitative measurements for western blot analysis. (A) Tau phosphorylated at S199/202 and S396 in SH-SY5Y cells after co-treatment with okadaic acid and mirodenafil (n=4). (B) Phosphorylated GSK-3β and phosphorylated Akt in SH-SY5Y cells after co-treatment with Aβ42, mirodenafil, and the PI3K inhibitor LY-294002 (n=4). (C) APP and BACE1 expression after co-treatment with Aβ42 and mirodenafil in HT-22 cells (n ≥ 5). (D) Phosphorylated AMPK and Aβ after co-treatment with Aβ42 and mirodenafil in SH-SY5Y cells (n=4). (E) The autophagy markers p62 and LC3B after co-treatment with Aβ42, mirodenafil, and autophagy inhibitor 3-MA (n=4) (F) GR after co-treatment with Aβ42 and mirodenafil in HT-22 cells. Data are presented as the mean ± SEM; *P < 0.05, **P < 0.01. All statistical comparisons were performed relative to Aβ42-treated cells. Statistical significance was assessed by one-way ANOVA followed by Bonferroni’s post hoc test for multiple comparisons. Figure S2. A. Mirodenafil impedes nuclear localization of GR homodimers after treatment with dexamethasone. HEK293 cells were transfected with Myc-tagged GR and GFP-tagged GR constructs. Following incubation for 24 h, Myc-tagged GR and GFP-tagged GR were detected by immunofluorescence confocal microscopy after co-treatment with dexamethasone and PDE5 inhibitors for 6 h. B. Quantification of nuclear localization of Myc-tagged GR and GFP-tagged GR after co-treatment with dexamethasone and PDE5 inhibitors. Immunofluorescence confocal images were obtained using LSM 800 confocal laser scanning microscopy (Zeiss). Mean fluorescence intensity in the nuclei and whole cells was measured using Zen Blue Edition software (Zeiss). Nuclear GR intensity was divided by total GR intensity to indicate relative distribution of Myc-GR and GFP-GR in nuclei and cytoplasm of HT-22 cells. (n>12). Data are presented as the mean ± SEM; *P < 0.05. All statistical comparisons were performed relative to Aβ42-treated cells. Statistical significance was assessed by one-way ANOVA followed by Bonferroni’s post hoc test for multiple comparisons. Figure S3. Real-time qRT-PCR for Wnts (Wnt1, Wnt3a, Wnt5a, and Wnt7a) after treatment with Aβ42 and mirodenafil for 6 h in HT-22 cells (n ≥ 5). Data are presented as the mean ± SEM; *P < 0.05, **P < 0.01. All statistical comparisons were performed relative to Aβ42-treated cells. Statistical significance was assessed by one-way ANOVA followed by Bonferroni’s post hoc test for multiple comparisons. Figure S4. Mirodenafil ameliorates AD pathology through multiple mechanisms of action. Representative schematic illustration of the possible mechanisms through which mirodenafil improves cognition and ameliorates AD pathology. Mirodenafil enhances neuronal survival through the activation of the cGMP/PKG/CREB signaling pathway, which upregulates the expression of neurotrophic factors, promotes the maintenance of the mitochondrial membrane potential, and prevents apoptotic cell death. The downregulation of GSK-3β activity contributes to the reduction of phosphorylated tau, whereas the amyloid-targeting properties of mirodenafil decrease the Aβ burden by modulating the production, aggregation, and clearance of Aβ. Additionally, mirodenafil activates Wnt/β-catenin signaling by downregulating the expression of the Wnt antagonist Dkk1 or repressing GR transcriptional activity.

Published
2022
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