• Title/Summary/Keyword: Sirt6

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Investigation of candidated genes for molecular characterization of DongGyeong dog populations (Gyeongju)

  • Park, Chang-Eun;Lee, Eun-Woo;Sung, Ki-Chang;Choi, Seog-Gyu
    • Korean Journal of Veterinary Service
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    • v.33 no.4
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    • pp.361-366
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    • 2010
  • This study was carried out to investigate the characters of short-tailed dogs (DongGyeong dogs) with anatomical insights, molecular genetics in Gyeongju. The present study was conducted to further characterize of short-tailed dog population in Gyeongju. The short-tailed dog was analyzed in the distribution of 55 individual. The anatomical insights were by x-ray. For discovery of specific genes expressions were measured by Hot-start PCR analysis. Anatomy survey, the number of vertebral typical consists of more than 20. 88.9% of short-tailed dog populations consists of 3-8 vertebrates. The 54 individuals of the 47 observe the vestigial tailed of the sacrum. No detected sacrococcygeal vertebrae degradation individuals were malformation defects. The 3 genes were DEGs (differentially expressed genes) in Dong-Gyeong dogs. We succeeded in finding 3 novel DongGyeong dogs specific genes by using Hot-start PCR analysis, this study suggests that these novel genes may play role (s) in DongGyeong dogs.

Monitoring Rock Physical Property Changes due to Excavations Using Horizontal Crosshole Georadar Tomography (수평 시추공간 지오레이다 토모그래피를 이용한 터널 굴착에 의한 암반 물성 변화의 고찰)

  • Jung, Yun-Moon;Lee, Myung-Sung;Song, Myung-Jun;Woo, Ik
    • Tunnel and Underground Space
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    • v.6 no.4
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    • pp.342-347
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    • 1996
  • The changes of electromagnetic wave velocity in rock were monitored to investigate rock behaviors due to the drill & blasting excavations through georadar tomography during the construction of the underground rock laboratory (5 m wide, 6 m high, and 140 m long) at Mabuk-Ri, Goosung-Myun, Yongin-Si, Kyunggi-Do. Two horizontal boreholes spaced 1.4 m apart were drilled parallel to the test tunnel before excavating it, high-resolution crosshole georadar tomography with about 500 MHz electromagnetic waves was performed at pre-excavation phase (May, 1996) and post-excavation phase (August, 1996). The data were acquired with the combination of 34 sources and 44 receivers with space of 0.3 m. Only 11 continuous receivers were selectively utilized with one fixed source. Sampling interval was 0.4 ns and each trace has 512 samples. The first arrival of each trace was picked manually with a picking software. The total number of rays used in inversion amounted to 34x11 and the size of pixel was determined to be 0.3 m. As an inversion technique, SIRT(Simultaneous Iterative Reconstruction Technique) was applied in this study. The velocity of electromagnetic waves at post-excavation phase decreased as large as 15% in comparison with that at pre-excavation phase, which may be attributed to the creation of micro-cracks in rock due to excavations and saturation with groundwater. Small amount of borehole deviation made a critical effect in radar tomography. Totally different tomograms were created after borehole deviation corrections.

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Ursolic acid improves the indoxyl sulfate-induced impairment of mitochondrial biogenesis in C2C12 cells

  • Sasaki, Yutaro;Kojima-Yuasa, Akiko;Tadano, Hinako;Mizuno, Ayaka;Kon, Atsushi;Norikura, Toshio
    • Nutrition Research and Practice
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    • v.16 no.2
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    • pp.147-160
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    • 2022
  • BACKGROUND/OBJECTIVES: Patients with chronic kidney disease (CKD) have a high concentration of uremic toxins in their blood and often experience muscle atrophy. Indoxyl sulfate (IS) is a uremic toxin produced by tryptophan metabolism. Although an elevated IS level may induce muscle dysfunction, the effect of IS on physiological concentration has not been elucidated. Additionally, the effects of ursolic acid (UA) on muscle hypertrophy have been reported in healthy models; however, it is unclear whether UA ameliorates muscle dysfunction associated with chronic diseases, such as CKD. Thus, this study aimed to investigate whether UA can improve the IS-induced impairment of mitochondrial biogenesis. MATERIALS/METHODS: C2C12 cells were incubated with or without IS (0.1 mM) and UA (1 or 2 μM) to elucidate the physiological effect of UA on CKD-related mitochondrial dysfunction and its related mechanisms using real-time reverse transcription-polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay. RESULTS: IS suppressed the expression of differentiation marker genes without decreasing cell viability. IS decreased the mitochondrial DNA copy number and ATP levels by downregulating the genes pertaining to mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam, Sirt1, and Mef2c), fusion (Mfn1 and Mfn2), oxidative phosphorylation (Cycs and Atp5b), and fatty acid oxidation (Pdk4, Acadm, Cpt1b, and Cd36). Furthermore, IS increased the intracellular mRNA and secretory protein levels of interleukin (IL)-6. Finally, UA ameliorated the IS-induced impairment in C2C12 cells. CONCLUSIONS: Our results indicated that UA improves the IS-induced impairment of mitochondrial biogenesis by affecting differentiation, ATP levels, and IL-6 secretion in C2C12 cells. Therefore, UA could be a novel therapeutic agent for CKD-induced muscle dysfunction.

Effects of Chaenomelis Fructus Extract on the regulation of myoblasts differentiation and the expression of biogenetic factors in C2C12 myotubes (모과추출물의 C2C12 근육세포에서 근분화 및 에너지대사조절인자 발현 증진 효과 연구)

  • Kang, Seok Yong;Hyun, Sun Young;Kwon, Yedam;Park, Yong-Ki;Jung, Hyo Won
    • The Korea Journal of Herbology
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    • v.34 no.6
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    • pp.99-107
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    • 2019
  • Objective : The present study was conducted to investigate the effects of Chaenomelis Fructus (CF) on the regulation of biogenesis in C2C12 mouse skeletal muscle cells. Methods : C2C12 myoblasts were differentiated into myotubes in 2% horse serum-containing medium for 5 days, and then treated with CF extract at different concentrations for 48 hr. The expression of muscle differentiation markers, myogenin and myosin heavy chain (MHC) and mitochondrial biogenesis-regulating factors, peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC1α), sirtuin1 (Sirt1), nuclear respiratory factor1 (NRF1) and transcription factor A, mitochondrial (TFAM), and the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) were determined in C2C12 myotubes by reverse transcriptase (RT)-polymerase chain reaction (RT-PCR) and western blot, respectively. The cellular glucose levels and total ATP contents were measured by cellular glucose uptake and ATP assays, respectively. Results : Treatment with CF extract (0.01, 0.02, and 0.05 mg/㎖) significantly increased the expression of MHC protein in C2C12 myotubes compared with non-treated cells. CF extract significantly increased the expression of PGC1α and TFAM in the myotubes. Also, CF extract significantly increased glucose uptake levels and ATP contents in the myotubes. Conclusion : CF extract can stimulate C2C12 myoblasts differentiation into myotubes and increase energy production through upregulation of the expression of mitochondrial biogenetic factors in C2C12 mouse skeletal muscle cell. This suggests that CF can help to improve skeletal muscle function with stimulation of the energy metabolism.

Study of the Effect and Underlying Mechanism of Clove Extract on Monosodium Iodoacetate-Induced Osteoarthritis in Rats (정향(丁香) 추출물이 골관절염 흰쥐에 미치는 효과 및 기전 연구)

  • Jin A Lee;Min Ju Kim;Seong-Wook Seo;Mi-Rae Shin
    • The Journal of Internal Korean Medicine
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    • v.43 no.6
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    • pp.1089-1104
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    • 2022
  • Objective: The aim of this study was to identify the efficacy and underlying mechanism of cloves as an osteoarthritis (OA) treatment in a monosodium iodoacetate (MIA)-induced rat OA model. Osteoarthritis (OA) is nowadays one of the most prevalent degenerative joint diseases. Methods: Sprague-Dawley rats treated with MIA (50 μL; 80 mg/mL) were used as in vivo OA models. Cloves (100 and 200 mg/kg b.w.) were administered orally once daily for 2 weeks from 7 days after MIA injection. Changes in hindpaw weight distribution (HWD) were measured as a joint discomfort index. Activation markers related to inflammatory responses and cartilage degeneration in the right knee joints were evaluated by serum analysis and western blotting. Results: HWD decreased in the MIA control group but showed a dose-dependent elevation after clove treatment. Clove treatment inhibited inflammatory factors by PI3K/Akt/NF-κB signaling pathways, while also activating antioxidant factors through Sirt1/AMPK signaling pathways. Clove treatment also suppressed matrix metalloproteinase (MMP) overexpression and significantly increased the levels of tissue inhibitors of metalloproteinases (TIMPs). Conclusions: Treatment with cloves effectively reversed MIA-induced effects. Therefore, clove treatment could have the potential to protect against or treat OA.

The Anti-Obesity Activity of Syzygium aromaticum L. in High-Fat Diet-induced Obese Mice (고지방식이로 유도된 비만 마우스에서 정향(丁香)의 항비만 효과)

  • Hui Yeon An;Seong-Soo Roh;Mi-Rae Shin
    • The Korea Journal of Herbology
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    • v.39 no.1
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    • pp.11-21
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    • 2024
  • Objectives : This study aims to analyze the anti-obesity effect of Syzygium aromaticum L. (SA) in obese mice made by a 60% high-fat diet (HFD). Methods : The antioxidant activities of SA were evaluated in vitro. To assess the anti-obesity effect of SA, male C57BL/6 mice were divided into five groups: Normal, Control, GC100 (Garcinia cambogia 100 mg/kg/day), SA100 (SA 100 mg/kg/day), SA200 (SA 200 mg/kg/day). All groups underwent a 6-week regimen of HFD and oral administration, except for the Normal group. Subsequently, we performed blood analysis, western blotting, and histopathological staining. Results : SA demonstrated effectiveness in antioxidant measurements. SA treatment resulted in a significant decrease in body weight gain, along with reductions in liver and epididymal fat weights. Serum triglyceride (TG), total cholesterol (TC), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and leptin levels were reduced with SA treatment. Moreover, in the SA100 group, the reduction of both TG and TC synthesis was caused by inhibiting the sterol regulatory element-binding transcription factor 1 (SREBP-1) and sterol regulatory element-binding transcription factor 2 (SREBP-2) through the Sirtuin 1 (Sirt1)/phospho-AMP-activated protein kinase (p-AMPK) pathway. Furthermore, SA treatment at a dose of 100 mg/kg reduced the accumulation of lipid droplets in the liver and the adipocyte size of the epididymal fat. Conclusion : Our research reveals the anti-obesity effects of SA by demonstrating its ability to inhibit body weight gain and lipid accumulation, suggesting that SA might be promising for obesity treatment.

Histone acetyltransferase inhibitors antagonize AMP-activated protein kinase in postmortem glycolysis

  • Li, Qiong;Li, Zhongwen;Lou, Aihua;Wang, Zhenyu;Zhang, Dequan;Shen, Qingwu W.
    • Asian-Australasian Journal of Animal Sciences
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    • v.30 no.6
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    • pp.857-864
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    • 2017
  • Objective: The purpose of this study was to investigate the influence of AMP-activated protein kinase (AMPK) activation on protein acetylation and glycolysis in postmortem muscle to better understand the mechanism by which AMPK regulates postmortem glycolysis and meat quality. Methods: A total of 32 mice were randomly assigned to four groups and intraperitoneally injected with 5-Aminoimidazole-4-carboxamide1-${\beta}$-D-ribofuranoside (AICAR, a specific activator of AMPK), AICAR and histone acetyltransferase inhibitor II, or AICAR, Trichostatin A (TSA, an inhibitor of histone deacetylase I and II) and Nicotinamide (NAM, an inhibitor of the Sirt family deacetylases). After mice were euthanized, the Longissimus dorsi muscle was collected at 0 h, 45 min, and 24 h postmortem. AMPK activity, protein acetylation and glycolysis in postmortem muscle were measured. Results: Activation of AMPK by AICAR significantly increased glycolysis in postmortem muscle. At the same time, it increased the total acetylated proteins in muscle 45 min postmortem. Inhibition of protein acetylation by histone acetyltransferase inhibitors reduced AMPK activation induced increase in the total acetylated proteins and glycolytic rate in muscle early postmortem, while histone deacetylase inhibitors further promoted protein acetylation and glycolysis. Several bands of proteins were detected to be differentially acetylated in muscle with different glycolytic rates. Conclusion: Protein acetylation plays an important regulatory role in postmortem glycolysis. As AMPK mediates the effects of pre-slaughter stress on postmortem glycolysis, protein acetylation is likely a mechanism by which antemortem stress influenced postmortem metabolism and meat quality though the exact mechanism is to be elucidated.

Ginseng seed oil ameliorates hepatic lipid accumulation in vitro and in vivo

  • Kim, Go Woon;Jo, Hee Kyung;Chung, Sung Hyun
    • Journal of Ginseng Research
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    • v.42 no.4
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    • pp.419-428
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    • 2018
  • Background: Despite the large number of studies on ginseng, pharmacological activities of ginseng seed oil (GSO) have not been established. GSO is rich in unsaturated fatty acids, mostly oleic and linoleic acids. Unsaturated fatty acids are known to exert a therapeutic effect in nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the protective effect and underlying mechanisms of GSO against NAFLD using in vitro and in vivo models. Methods: In vitro lipid accumulation was induced by free fatty acid mixture in HepG2 cells and by 3 wk of high fat diet (HFD)-feeding in Sprague-Dawley rats prior to hepatocyte isolation. The effects of GSO against diet-induced hepatic steatosis were further examined in C57BL/6J mice fed a HFD for 12 wk. Results: Oil Red O staining and intracellular triglyceride levels showed marked accumulation of lipid droplets in both HepG2 cells and rat hepatocytes, and these were attenuated by GSO treatment. In HFD-fed mice, GSO improved HFD-induced dyslipidemia and hepatic insulin resistance. Increased hepatic lipid contents were observed in HFD-fed mice and it was lowered in GSO (500 mg/kg)-treated mice by 26.4% which was evident in histological analysis. Pathway analysis of hepatic global gene expression indicated that GSO increased the expression of genes associated with ${\beta}$-oxidation (Ppara, Ppargc1a, Sirt1, and Cpt1a) and decreased the expression of lipogenic genes (Srebf1 and Mlxipl), and these were confirmed with reverse transcription and quantitative polymerase-chain reaction. Conclusion: These findings suggest that GSO has a beneficial effect on NAFLD through the suppression of lipogenesis and stimulation of fatty acid degradation pathway.

Anti-proliferative and Apoptotic Activity of Extracts of Lindera glauca Blume root in Human HCT116 Colorectal Cancer Cells (감태나무 뿌리 추출물에 의한 대장암세포의 성장억제 및 세포사멸유도)

  • Kim, Yeah-Un;Moon, Ha-Rin;Han, Inhwa;Yun, Jung-Mi
    • Journal of the Korean Society of Food Culture
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    • v.36 no.2
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    • pp.235-245
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    • 2021
  • Lindera glauca Blume has been used in Korean traditional medicine to treat the symptoms of paralysis, abdominal pain, speech disorders, extravasations, contusions, and pain caused by rheumatoid arthritis. We investigated the effect of L. glauca Blume extracts on the proliferation of colorectal cancer cells in vitro using HCT116 human colorectal cancer cell lines. We also investigated its mechanism of action. For this purpose, we used the MTT assay, western blotting, DNA fragmentation analysis, and flow cytometry. HCT116 cells were cultured in several concentrations of ethanol extracts of L. glauca Blume root (0, 50, 100 ㎍/mL). In this study, colon cancer cell growth was inhibited by L. glauca Blume root extract in a dose-dependent manner. It was associated with induction of apoptosis as assessed by nuclear fragmentation and cell cycle analysis. Apoptosis was assessed using western blotting for TNF-α, IL-6, NF-κB, Caspase-3, PARP, Bax, Bcl-2, and SIRT1. The extract also dose-dependently upregulated the expression Bax, the pro-apoptotic gene and downregulated the expression of the anti-apoptotic gene Bcl-2. Furthermore, the extract enhanced Caspase-3 activity in a dose-dependent manner. Our findings provide evidence that L. glauca Blume extract may mediate its anti-proliferative effect via the modulation of apoptosis.

Recombinant Human HAPLN1 Mitigates Pulmonary Emphysema by Increasing TGF-β Receptor I and Sirtuins Levels in Human Alveolar Epithelial Cells

  • Yongwei Piao;So Yoon Yun;Zhicheng Fu;Ji Min Jang;Moon Jung Back;Ha Hyung Kim;Dae Kyong Kim
    • Molecules and Cells
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    • v.46 no.9
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    • pp.558-572
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    • 2023
  • Chronic obstructive pulmonary disease (COPD) will be the third leading cause of death worldwide by 2030. One of its components, emphysema, has been defined as a lung disease that irreversibly damages the lungs' alveoli. Treatment is currently unavailable for emphysema symptoms and complete cure of the disease. Hyaluronan (HA) and proteoglycan link protein 1 (HAPLN1), an HA-binding protein linking HA in the extracellular matrix to stabilize the proteoglycan structure, forms a bulky hydrogel-like aggregate. Studies on the biological role of the full-length HAPLN1, a simple structure-stabilizing protein, are limited. Here, we demonstrated for the first time that treating human alveolar epithelial type 2 cells with recombinant human HAPLN1 (rhHAPLN1) increased TGF-β receptor 1 (TGF-β RI) protein levels, but not TGF-β RII, in a CD44-dependent manner with concurrent enhancement of the phosphorylated Smad3 (p-Smad3), but not p-Smad2, upon TGF-β1 stimulation. Furthermore, rhHAPLN1 significantly increased sirtuins levels (i.e., SIRT1/2/6) without TGF-β1 and inhibited acetylated p300 levels that were increased by TGF-β1. rhHAPLN1 is crucial in regulating cellular senescence, including p53, p21, and p16, and inflammation markers such as p-NF-κB and Nrf2. Both senile emphysema mouse model induced via intraperitoneal rhHAPLN1 injections and porcine pancreatic elastase (PPE)-induced COPD mouse model generated via rhHAPLN1-containing aerosols inhalations showed a significantly potent efficacy in reducing alveolar spaces enlargement. Preclinical trials are underway to investigate the effects of inhaled rhHAPLN1-containing aerosols on several COPD animal models.