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Fluoxetine-induced abnormalities of cardiac function
Mun Young Lee, Gi Beum Kim, Hyung Sub Kang, Jin Shang Kim, Shang Jin Kim 대한수의학회 대한수의학회 학술대회발표집 2 Pages
대한수의학회 대한수의학회 학술대회발표집 추계학술심포지움 264 336-337 (2 pages)
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Effect of phosphorus deficiency on erythrocytic morphology and function in cows
Ziwei Zhang, Mingyu Bi, Jie Yang, Haidong Yao, Zhonghua Liu, Shiwen Xu 대한수의학회 Journal of Veterinary Science 8 Pages
대한수의학회 Journal of Veterinary Science 2017, 제 18권 제 3호 10 333-340 (8 pages)
The aim of this study was to evaluate the influence of phosphorus (P) deficiency on the morphological and functional characteristics of erythrocytes in cows. Forty Holstein-Friesian dairy cows in mid-lactation were randomly divided into two groups of 20 each and were fed either a low-P diet (0.03% P/kg dry matter [DM]) or a control diet (0.36% P/kg DM). Red blood cell (RBC) indices results showed RBC and mean corpuscular hemoglobin decreased while mean corpuscular volume increased significantly... -
Alterations in antioxidant function and cell apoptosis in duck spleen exposed to molybdenum and/or cadmium
Mengmeng Zhang, Junrong Luo, Caiying Zhang, Huabin Cao, Bing Xia, Guoliang Hu 대한수의학회 Journal of Veterinary Science 8 Pages
대한수의학회 Journal of Veterinary Science 2017, 제 18권 제 2호 9 193-200 (8 pages)
and xanthine oxidase and catalase activities decreased in the Mo and/or Cd groups compared with levels in the control group. Bak-1 and Caspase-3 expressions were upregulated in the high Mo + Cd group, while Bcl-2 was downregulated. In addition, mitochondrial crest fracture, swelling, vacuolation, deformed nuclei, and karyopyknosis in both Mo + Cd treated groups were more severe than in the other groups. The results suggest that Mo and/or Cd can induce oxidative stress and apoptosis of spleen via... -
Gossypol acetic acid induces apoptosis in RAW264.7 cells via a caspase-dependent mitochondrial signaling pathway
Sijun Deng, Hui Yuan, Jine Yi, Yin Lu, Qiang Wei, Chengzhi Guo, Jing Wu, Liyun Yuan, Zuping He 대한수의학회 Journal of Veterinary Science 9 Pages
대한수의학회 Journal of Veterinary Science 2013, 제 14권 제 3호 7 281-289 (9 pages)
TUNEL assay, acridine orange/ethidium bromide staining and flow cytometry. Moreover, mitochondrial membrane potential (ΔΨm) with Rhodamine 123 and reactive oxygen species (ROS) with DCFH-DA were analyzed by fluorescence spectrofluorometry. In addition, the expression of caspase-3 and caspase-9 was assessed by Western Blot assay. Finally, the GA-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK, respectively. GA significantly... -
Effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and endoplasmic reticulum stress of the cardiac muscle in obese middle-aged rats
KijinKim, NayoungAhn, SuryunJung, SoleePark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2017, Vol.21 No.6 8 633-641 (9 pages)
The aim of this study is to investigate the effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and ER stress of the cardiac muscle in high fat diet-induced obese middle-aged rats. We induced obesity over 6 weeks of period in 40 male Sprague-Dawley rats around 50 weeks old, and were randomly divided into four experimental groups: chow, HFD, exercise+HFD, and exercise+chow. The exercising groups underwent high-intensity intermittent training using a... -
Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle
Jun-WonHeo, Mi-HyunNo, Dong-HoPark, Ju-HeeKang, DaeYunSeo, JinHan, P.DarrellNeufer, Hyo-BumKwak 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 11 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2017, Vol.21 No.6 1 567-577 (11 pages)
Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes.... -
Protein kinase C beta II upregulates intercellular adhesion molecule-1 via mitochondrial activation in cultured endothelial cells
HeeKyoungJoo, YuRanLee, SungaChoi, MyoungSooPark, GunKang, Cuk-SeongKim, ByeongHwaJeon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2017, Vol.21 No.4 3 377-384 (8 pages)
ICAM-1, and p66shc phosphorylation in cultured endothelial cells. Finally, PKCβII-induced ICAM-1 expression was inhibited by Mito-TEMPO, a mitochondrial ROS scavenger, suggesting the involvement of mitochondrial ROS in PKC-induced vascular inflammation. Taken together, the results suggest that PKCβII plays an important role in PMA-induced endothelial dysfunction, and that the inhibition of PKCβII-dependent p66shc signaling acts as a therapeutic target for vascular inflammatory diseases. -
Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension
TongZhou, HaiyangTang, YingHan, DustinFraidenburg, Young-WonKim, DongheeLee, JeongyoonChoi, HyoweonBang, Jae-HongKo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2017, Vol.21 No.3 10 353-360 (8 pages)
Several human diseases have been associated with mitochondrial voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we...


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