• 제목/요약/키워드: Fat-suppression

검색결과 106건 처리시간 0.034초

귀전우(鬼箭羽)(Euonymus alatus(Thunb.) Sieb)가 간암세포(肝癌細胞)(Hep3B)와 자궁암세포(子宮癌細胞)(HeLa)의 성장억제(成長抑制)에 미치는 영향(影響)에 관한 연구(硏究) (Effect of Growth Inhibition in Hep3B cell and HeLa cell by treatment of Euonymus alatus(Thunb.) Sieb extracts)

  • 최달영
    • 동국한의학연구소논문집
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    • 제7권2호
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    • pp.155-162
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    • 1999
  • 귀전우(Euonymus alatus Sieb.)가 간암, 식도암, 위암, 자궁암등의 각종 암을 치료하는 방법으로 민방에서 많이 사용하고 있다. 실제 Euonymus alatus(Thumb.) Sieb의 추출물중 Eupolyphaga simensis(ES)는 HDL-C/TC ratio와 LCATactivity를 증진시킨다. Human hepatoblastoma 세포인 Hep3B 세포의 성장억제를 유도하는 factor로는 TGF-${\beta}$, Insulin 등으로 알려져 있다. 따라서 귀전우는 간에 있어 당 대사에 관여하는 plasma HDL3-C level은 낮게 유지함으로써 간에서 지방간 이행을 억제 하여 간에서의 암 발생을 억제하는 효과를 보인다. 실험에서 귀전우가 자궁암세포보다도 간암세포에 보다 높은 세포독성을 보임으로써 여러종류의 암에 모두 적용하기는 어렵다고 보여진다. 또한 귀전우가 바이러스에 의해 유도되는 간암과 hepatocellular Carcinoma 세포에서 효과가 있는지와 HCC에서 세포의 증식억제효과를 어떤 경로를 통해 이루어지는지 계속적으로 연구가 수행되어져야 될 것이다.

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Suppression of Hepatic Lipogenic Enzyme by Dietary Fish Oil In Rat Hepatocarcinogenesis

  • Kim, Hye-Kyeong;Choi, Hay-Mie;,
    • Toxicological Research
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    • 제14권3호
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    • pp.285-291
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    • 1998
  • This study was designed to examine the effects of polyundaturated fatty acid(PUFA) from different sourecs on hepatic lipogenic enzyme and peroxisomal ${\beta}$-oxidation in murine hepatocarcinogenesis initiated by diethylnitrodamine (DEN). Male Sprague-Dawley rats were fed one of three diets containing 10%(w/w)fat; fish oil-corn oil blended(FO), corn oil-beef tallow-fish oil blended(CF), or corn oil-beef tallow-perilla oil blended (CP), from the gestation period. At 10 weeks, animals were received a single inraperitoneal injection of DEN (200mg/kg body weight), were subjected to two-thirds partial hepatectomy 3 weeks later and were sacrificed 8 weeks after DEN initiation. The areas of placental glutathione S-transferase (GST-P) positive foci were significantly smaller in rats fed fish oil containing diets (FO and CF) than those fed CP diet. Fish oil feeding significantly decreased th activities of lipogenic enzyme. Rats fed fish oil containing diets (FO, CF) exhibited the lower fatty acid synthase (FAS) activity than those fed CP diet and FAS activity was positively correlated with areas of GSP-P positivie foci. Glucose-6-phophate dehydrogenase activity was the lowest and peroxisomal ${\beta}$-oxidation was stimulated in rats fed FO diet compared to other groups. It was also found that serum cholesterol was decreased in FO group. Therefore, the preventive effect against hepatocarcinogenesis and hypolipidemic effect of fish oil can be explained partly by suppression of the hepatic lipogenesis and by increase of peroxisomal ${\beta}$-oxidation.

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Ginsenoside compound K ameliorates palmitate-induced atrophy in C2C12 myotubes via promyogenic effects and AMPK/autophagy-mediated suppression of endoplasmic reticulum stress

  • Kim, Tae Jin;Pyun, Do Hyeon;Kim, Myeong Jun;Jeong, Ji Hoon;Abd El-Aty, A.M.;Jung, Tae Woo
    • Journal of Ginseng Research
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    • 제46권3호
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    • pp.444-453
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    • 2022
  • Background: Compound K (CK) is among the protopanaxadiol (PPD)-type ginsenoside group, which produces multiple pharmacological effects. Herein, we examined the effects of CK on muscle atrophy under hyperlipidemic conditions along with its pro-myogenic effects. Further, the molecular pathways underlying the effects of CK on skeletal muscle have been justified. Methods: C2C12 myotubes were treated with palmitate and CK. C2C12 myoblasts were differentiated using CK for 4-5 days. For the in vivo experiments, CK was administered to mice fed on a high-fat diet for 8 weeks. The protein expression levels were analyzed using western blotting analysis. Target protein suppression was performed using small interfering (si) RNA transfection. Histological examination was performed using Jenner-Giemsa and H&E staining techniques. Results: CK treatment attenuated ER stress markers, such as eIF2a phosphorylation and CHOP expression and impaired myotube formation in palmitate-treated C2C12 myotubes and skeletal muscle of mice fed on HFD. CK treatment augmented AMPK along with autophagy markers in skeletal muscle cells in vitro and in vivo experiments. AMPK siRNA or 3-MA, an autophagy inhibitor, abrogated the impacts of CK in C2C12 myotubes. CK treatment augmented p38 and Akt phosphorylation, leading to an enhancement of C2C12 myogenesis. However, AMPK siRNA abolished the effects of CK in C2C12 myoblasts. Conclusion: These findings denote that CK prevents lipid-induced skeletal muscle apoptosis via AMPK/autophagy-mediated attenuation of ER stress and induction of myoblast differentiation. Therefore, we may suggest the use of CK as a potential therapeutic approach for treating muscle-wasting conditions associated with obesity.

Wnt/β-catenin signaling activator restores hair regeneration suppressed by diabetes mellitus

  • Yeong Chan, Ryu;You-rin, Kim;Jiyeon, Park;Sehee, Choi;Geon-Uk, Kim ;Eunhwan, Kim;Yumi, Hwang;Heejene, Kim;Soon Sun, Bak;Jin Eun, Lee;Young Kwan, Sung;Gyoonhee, Han;Soung-Hoon, Lee;Kang-Yell, Choi
    • BMB Reports
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    • 제55권11호
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    • pp.559-564
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    • 2022
  • Diabetes mellitus is one of the most prevalent diseases in modern society. Many complicationssuch as hepatic cirrhosis, neuropathy, cardiac infarction, and so on are associated with diabetes. Although a relationship between diabetes and hair loss has been recently reported, the treatment of diabetic hair loss by Wnt/β-catenin activators has not been achieved yet. In this study, we found that the depilation-induced anagen phase was delayed in both db/db mice and high-fat diet (HFD) and streptozotocin (STZ)-induced diabetic mice. In diabetic mice, both hair regrowth and wound-induced hair follicle neogenesis (WIHN) were reduced because of suppression of Wnt/β-catenin signaling and decreased proliferation of hair follicle cells. We identified that KY19382, a small molecule that activates Wnt/β-catenin signaling, restored the capabilities of regrowth and WIHN in diabetic mice. The Wnt/β-catenin signaling activator also increased the length of the human hair follicle which was decreased under high glucose culture conditions. Overall, the diabetic condition reduced both hair regrowth and regeneration with suppression of the Wnt/β-catenin signaling pathway. Consequently, the usage of Wnt/β-catenin signaling activators could be a potential strategy to treat diabetes-induced alopecia patients.

Dietary Aloe Reduces Adipogenesis via the Activation of AMPK and Suppresses Obesity-related Inflammation in Obese Mice

  • Shin, Eun-Ju;Shin, Seul-Mee;Kong, Hyun-Seok;Lee, Sung-Won;Do, Seon-Gil;Jo, Tae-Hyung;Park, Young-In;Lee, Chong-Kil;Hwang, In-Kyeong;Kim, Kyung-Jae
    • IMMUNE NETWORK
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    • 제11권2호
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    • pp.107-113
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    • 2011
  • Background: Metabolic disorders, including type II diabetes and obesity, present major health risks in industrialized countries. AMP-activated protein kinase (AMPK) has become the focus of a great deal of attention as a novel therapeutic target for the treatment of metabolic syndromes. In this study, we evaluated whether dietary aloe could reduce obesity-induced inflammation and adipogenesis. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM complex downregulated fat size through suppressed expression of scavenger receptors on adipose tissue macrophages (ATMs) compared with HFD. Both white adipose tissue (WATs) and muscle exhibited increased AMPK activation through aloe supplementation, and in particular, the Aloe QDM complex. Obesity-induced inflammatory cytokines (IL-$1{\beta}$ and -6) and $HIF1{\alpha}$ mRNA and protein were decreased markedly, as was macrophage infiltration by the Aloe QDM complex. Further, the Aloe QDM complex decreased the translocation of NF-${\kappa}B$ p65 from the cytosol in the WAT. Conclusion: Dietary aloe formula reduced obesity-induced inflammatory responses by activation of AMPK in muscle and suppression of proinflammatory cytokines in the WAT. Additionally, the expression of scavenger receptors in the ATM and activation of AMPK in WAT led to reduction in the percent of body fat. Thus, we suggest that the effect of the Aloe QDM complex in the WAT and muscle are related to activation of AMPK and its use as a nutritional intervention against T2D and obesity-related inflammation.

활성 락토페린을 첨가한 저지방 세절소시지의 냉장 저장(8°C)중 이화학적, 조직적 및 저장 특성 (Physicochemical and Textural Properties, and Shelf-Life Effects of Low-fat Sausages Manufactured with Various Levels of Activated Lactoferrin during Refrigerated Storage)

  • 강인혜;이홍철;진구복
    • 한국축산식품학회지
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    • 제28권4호
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    • pp.408-414
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    • 2008
  • 본 연구에서 제조한 저지방 훈연 소시지는 활성락토페린을 각각 0, 0.3 및 0.6%로 함량을 달리하였고, 냉장저장($8^{\circ}C$)중 이화학적 및 조직학적 특성과 접종 미생물의 성장에 미치는 영향을 조사하기 위해 실시하였다 제조된 저지방 훈연소시지의 pH, 수분, 지방, 및 단백질의 함량은 각각 6.04-6.08, 72-76%, 1-2%, 12-14%로 처리구별 유의적인 차이가 없었다(p>0.05). 활성락토페린을 0.6% 첨가한 처리구는 0.3% 첨가구와 달리 무첨가 대조구에 비해 미생물의 성장을 억제하였으며(p<0.05), 유의적으로 높은 부서짐성을 보였다. 그러나 젖산나트륨 3.3%를 첨가에 의한 항균활성 효과보다는 낮은 효과로 평가되었다. 이상의 결과를 종합해 본 결과 락토페린은 육제품에 있어서 이화학적 및 조직학적성상에 거의 영향을 주지 않으면서 항균활성을 부여하는 좋은 기능성 물질로서 이용할 수 있을 것으로 판단된다.

고지방식이를 급여한 비만 마우스에서 luteolin이 화학적으로 유도한 대장암 발생에 미치는 영향 (Effects of luteolin on chemical induced colon carcinogenesis in high fat diet-fed obese mouse)

  • 박정은;김은정
    • Journal of Nutrition and Health
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    • 제51권1호
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    • pp.14-22
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    • 2018
  • 본 연구는 LUT이 고지방식이로 비만이 유도된 C57BL/6 마우스의 대장암 발생에 미치는 영향을 분석하기 위해 실험동물을 각 10마리씩 정상식이 (ND)군, 고지방식이 (HFD)군, HFD + 0.0025% LUT 보충 (HFD LL)군, 그리고 HFD + 0.005% LUT 보충 (HFD HL)군의 4군으로 분류하였다. 각 실험군은 AOM을 1회 복강 주사하고 AOM 투여 1주일 후 총 3 cycle의 1 ~ 2% 농도의 DSS를 음용수로 공급하여 대장암을 유발하였다. 실험식이는 AOM 발암시점부터 총 11주간 급여하였다. 연구결과, 군간 식이섭취량의 차이는 없었으나 HFD 급여군에서 체중과 식이효율의 유의적인 증가가 나타났으며 HFD군과 비교했을 때 LUT 보충에 따른 체중의 변화는 없었다. 그러나 LUT 보충은 ND군에 비해 HFD군에서 나타난 대장 무게/길이 비, 대장종양 수, 혈장 $TNF-{\alpha}$ 농도, 대장 iNOS와 COX-2 발현을 유의적으로 감소시켰으며 그 효과는 HFD HL군이 HFD LL군보다 높았다. 이러한 결과는 체중조절과는 별개로 LUT이 고지방식이에 의한 대장의 염증반응 억제를 통하여 비만과 연관된 대장암 발생을 억제할 수 있음을 제시하며 향후 비만에 의한 인슐린 저항성 및 adipokine 분비, 그리고 장내 균총 변화에 따른 대장 점막세포 증식과 대장암 발생에 LUT이 어떤 영향을 미치는지에 대한 연구를 더 깊이 있게 수행한다면 비만으로 인한 대장암 발생에 LUT이 효과적인 화학적 예방 (chemoprevention)제로 활용될 수 있을 것으로 기대한다.

Dietary Aloe Improves Insulin Sensitivity via the Suppression of Obesity-induced Inflammation in Obese Mice

  • Shin, Eun-Ju;Shim, Kyu-Suk;Kong, Hyun-Seok;Lee, Sung-Won;Shin, Seul-Mee;Kwon, Jeung-Hak;Jo, Tae-Hyung;Park, Young-In;Lee, Chong-Kil;Kim, Kyung-Jae
    • IMMUNE NETWORK
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    • 제11권1호
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    • pp.59-67
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    • 2011
  • Background: Insulin resistance is an integral feature of metabolic syndromes, including obesity, hyperglycemia, and hyperlipidemia. In this study, we evaluated whether the aloe component could reduce obesity-induced inflammation and the occurrence of metabolic disorders such as blood glucose and insulin resistance. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM lowered fasting blood glucose and plasma insulin compared with HFD. Obesity-induced inflammatory cytokine (IL-$1{\beta}$, -6, -12, TNF-${\alpha}$) and chemokine (CX3CL1, CCL5) mRNA and protein were decreased markedly, as was macrophage infiltration and hepatic triglycerides by Aloe QDM. At the same time, Aloe QDM decreased the mRNA and protein of $PPAR{\gamma}/LXR{\alpha}$ and $11{\beta}$-HSD1 both in the liver and WAT. Conclusion: Dietary aloe formula reduces obesity-induced glucose tolerance not only by suppressing inflammatory responses but also by inducing anti-inflammatory cytokines in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The effect of Aloe QDM complex in the WAT and liver are related to its dual action on $PPAR{\gamma}$ and $11{\beta}$-HSD1 ression and its use as a nutritional intervention against T2D and obesity-related inflammation is suggested.

Development of a Simultaneous Analytical Method for Diquat, Paraquat and Chlormequat in Animal Products Using UPLC-MS/MS

  • Cho, Il Kyu;Rahman, Md. Musfiqur;Seol, Jae Ung;Noh, Hyun Ho;Jo, Hyeong-Wook;Moon, Joon-Kwan
    • 한국환경농학회지
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    • 제39권4호
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    • pp.368-374
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    • 2020
  • BACKGROUND: The residual analysis of polar pesticides has remained a challenge. It is even more difficult to simultaneously analyze multiple polar pesticides. Diquat, paraquat, and chlormequat are typical examples of highly polar pesticides. The existing methods for the analysis of diquat, paraquat and chlormequat are complex and time consuming. Therefore, a simple, quick and effective method was developed in the represent study for simultaneous analysis of diquat, paraquat and chlormequat in animal products, meat and fat using UPLC-MS/MS. METHODS AND RESULTS: Sample extraction was carried out using acidified acetonitrile and water and re- extracted with acidified acetonitrile and combine the extracts followed by centrifugation. The extract was then cleaned up with a HLB cartridge after reconstitution with acidic acetonitrile and water. The method was validated in quintuplicate at three different concentrations. The limits of detection (LOD) and quantification (LOQ) were 0.0015 and 0.005 mg/L, respectively. Matrix suppression effect was observed for all of the analytes. A seven point matrix matched calibration curve was constructed for each of the compound resulted excellent linearity with determination coefficients (R2) ≥ 0.991. Accuracy and precision of the method was calculated from the recovery and repeatability and ranged from 62.4 to 119.7% with relative standard deviation less than 18.8%. CONCLUSION: The recovery and repeatability of the developed method were in the acceptable range according to the Codex Alimentarius guideline. The developed method can be applied for the routine monitoring of diquat, paraquat, and chlormequat in animal products, meat and fat.

Oxymatrine inhibits the pyroptosis in rat insulinoma cells by affecting nuclear factor kappa B and nuclear factor (erythroid-derived 2)-like 2 protein/heme oxygenase-1 pathways

  • Gao, Jingying;Xia, Lixia;Wei, Yuanyuan
    • The Korean Journal of Physiology and Pharmacology
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    • 제26권3호
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    • pp.165-174
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    • 2022
  • As the mechanism underlying glucose metabolism regulation by oxymatrine is unclear, this study investigated the effects of oxymatrine on pyroptosis in INS-1 cells. Flow cytometry was employed to examine cell pyroptosis and reactive oxygen species (ROS) production. Cell pyroptosis was also investigated via transmission electron microscopy and lactate dehydrogenase (LDH) release. Protein levels were detected using western blotting and interleukin (IL)-1β and IL-18 secretion by enzyme-linked immunosorbent assay. The caspase-1 activity and DNA-binding activity of nuclear factor kappa B (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 protein (Nrf2) were also assessed. In the high glucose and high fat-treated INS-1 cells (HG + PA), the caspase-1 activity and LDH content, as well as Nod-like receptor family pyrin domain containing 3, Gsdmd-N, caspase-1, apoptosis-associated speck-like protein containing a CARD, IL-1β, and IL-18 levels were increased. Moreover, P65 protein levels increased in the nucleus but decreased in the cytoplasm. Oxymatrine attenuated these effects and suppressed high glucose and high fat-induced ROS production. The increased levels of nuclear Nrf2 and heme oxygenase-1 (HO-1) in the HG + PA cells were further elevated after oxymatrine treatment, whereas cytoplasmic Nrf2 and Keleh-like ECH-associated protein levels decreased. Additionally, the elevated transcriptional activity of p65 in HG + PA cells was reduced by oxymatrine, whereas that of Nrf2 increased. The results indicate that the inhibition of pyroptosis in INS-1 cells by oxymatrine, a key factor in its glucose metabolism regulation, involves the suppression of the NF-κB pathway and activation of the Nrf2/HO-1 pathway.