K1-Fluo 相关文献推荐 （2021）

1.      Specific Pyruvate Kinase M2 Inhibitor, Compound 3K, Induces Autophagic Cell Death through Disruption of the Glycolysis Pathway in Ovarian Cancer Cells

Publication date: May 05, 2021

Jae Hyeon Park, Amit Kundu, Su Hyun Lee, ChunXue Jiang, Song Hee Lee, Ye Seul Kim, So Young Kyung, So Hyun Park, Hyung Sik Kim

摘要:

Ovarian cancer is a common cause of death among gynecological cancers. Although ovarian cancer initially responds to chemotherapy, frequent recurrence in patients remains a therapeutic challenge. Pyruvate kinase M2 (PKM2) plays a pivotal role in regulating cancer cell survival. However, its therapeutic role remains unclear. Here, we investigated the anticancer effects of compound 3K, a specific PKM2 inhibitor, on the regulation of autophagic and apoptotic pathways in SK-OV-3 (PKM2-overexpressing human ovarian adenocarcinoma cell line). The anticancer effect of compound 3K was examined using MTT and colony formation assays in SK-OV-3 cells. PKM2 expression was positively correlated with the severity of the tumor, and expression of pro-apoptotic proteins increased in SK-OV-3 cells following compound 3K treatment. Compound 3K induced AMPK activation, which was accompanied by mTOR inhibition. Additionally, this compound inhibited glycolysis, resulting in reduced proliferation of SK-OV-3 cells. Compound 3K treatment suppressed tumor progression in an in vivo xenograft model. Our findings suggest that the inhibition of PKM2 by compound 3K affected the Warburg effect and induced autophagic cell death. Therefore, use of specific PKM2 inhibitors to block the glycolytic pathway and target cancer cell metabolism represents a promising therapeutic approach for treating PKM2-overexpressing ovarian cancer

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关键词：Ovarian Cancer Cells

2.      Transcriptional profiling of mouse cavernous pericytes under high-glucose conditions: Implications for diabetic angiopathy

Publication date: June 02, 2021

Guo Nan Yin1, Jitao Wu2, Yuanshan Cui2 , Chunhua Lin2 , Lei Shi2 , Zhen-Li Gao2 , Jun-Kyu Suh1 , Ji-Kan Ryu1 , Hai-Rong Jin2

介绍：

Diabetes mellitus (DM) causes erectile dysfunction (ED) with severe angiopathy, which is the main reason for the reduced efficacy of phosphodiesterase-5 (PDE5) inhibitors in DM. Several studies have presented gene expression profiles of cavernosum tissue and cavernous endothelial cells in diabetes-induced ED , but the genetic mechanisms responsible have yet to be elucidated and more molecular candidates are needed. Pericytes are multifunctional mural cells that surround endothelial cells and support vascular development and homeostasis. Accumulating evidence shows that pericytes play important roles in vascular contractility and constitute a reservoir of mesenchymal stem cells. In mouse cavernosum tissue, we found that the distribution of pericytes protrudes more into in the micro vessels of the subtunical area than in the cavernous sinusoids. As we know, oxidized low-density lipoprotein (LDL) mediates oxidative stress and can induce pericyte apoptosis and diabetic retinopathy. We recently observed that a loss of pericytes increases the leakage of oxidized LDL in mice with diabetes-induced ED, which may hinder the expansion of erectile tissue by inducing cavernous inflammation and fibrosis in vivo and in vitro. Restoration of the cavernous pericyte content by injection of hepatocyte growth factor significantly decreases cavernous vascular permeability. However, the detailed functional roles of pericytes in penile erection are still largely unknown. Physiologic and pathologic gene expression profiling provides a means of understanding the molecular mechanisms underlying diabetes-induced ED and of identifying novel treatment targets. In the present study, we performed a microarray assay on mouse cavernous pericytes (MCPs) exposed to normal-glucose (NG, 5 mM) or high-glucose (HG, 30 mM) conditions, which were used to mimic diabetes-induced angiopathy, and we identified genes differentially induced in MCPs under these conditions. After screening for significantly altered genes, Hebp1 was chosen as a potential novel therapeutic candidate for diabetes-induced ED.

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关键词：Diabetes mellitus; Erectile dysfunction; Gene expression; Microarray analysis

3.      Effects of taurine and ginseng extracts on energy metabolism during exercise and their anti-fatigue properties in mice

Publication Date: January 15, 2021

Jisu Kim, Suji Beak, Sanghyun Ahn , Byung Seok Moon, Bom Sahn Kim , Sang Ju Lee , Seung Jun Oh , Hun-Young Park, Seung Hae Kwon, Chul Ho Shin, Kiwon Lim, and Kang Pa Lee

摘要:

BACKGROUND/OBJECTIVES: Ginseng extract (GSE) and taurine (TR) are widely used antifatigue resources in functional foods. However, the mechanism underlying the antifatigue effects of GSE and TR are still unclear. Hence, we investigated whether GSE and TR have synergistic effects against fatigue in mice. MATERIALS/METHODS: L6 cells were treated with different concentrations of TR and GSE, and cell viability was determined using 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfopheny)-2H-tetrazolium. Oxidative stress was analyzed by immunocytochemistry using MitoTracker Red FM and an anti-8-oxoguanine antibody. Respiratory gas analysis was performed to investigate metabolism. Expression of an activated protein kinase was analyzed using immunohistochemistry. Gene expression of cluster of differentiation 36 and pyruvate dehydrogenase lipoamide kinase isozyme 4 was measured using reverse transcription– polymerase chain reaction. Mice were orally administered TR, GSE, or their combination for 30 days, and then fatigue-related parameters, including lactate, blood urea nitrogen, and glycogen, were measured after forced swimming. RESULTS: TR and GSE reduced oxidative stress levels in hydrogen peroxide-stimulated L6 cells and enhanced the oxygen uptake and lipid metabolism in mice after acute exercise. After oral administration of TR or GSE for 30 days, the fatigue-related parameters did not change in mice. However, the mice administered GSE (400 mg/kg/day) alone for 30 days could swim longer than those from the other groups. Further, no synergistic effect was observed after the swimming exercise in mice treated with the TR and GSE combination for 30 days. CONCLUSIONS: Taken together, our data suggest that TR and GSE may exert antifatigue effects in mice after acute exercise by enhancing oxygen uptake and lipid oxidation.

涉及技术：K1-Fluo 激光荧光共聚焦技术

关键词：Fatigue; ginseng; taurine; exercise; lipid metabolism

4.      Korean Red Ginseng affects ovalbumin-induced asthma by modulating IL-12, IL-4, and IL-6 levels and the NF-kB/COX-2 and PGE2 pathways

Publication date: July , 2021

Soon-Young Lee, Min-Hee Kim, Seung-Hyun Kim, Taeho Ahn , Sung-Won Kim, Yi-Seong Kwak, Ik-Hyun Cho , Seung-Yeol Nah , Seung-Sik Cho, Kyung Mok Park , Dae-Hun Park, Chun-Sik Bae

摘要:

Background: Asthma is an incurable hyper-responsive disease of the pulmonary system that is caused by various allergens, including indoor and outdoor stimulators. According to the Global Asthma Network, 339 million people suffered from asthma in 2018, with particularly severe forms in children. Numerous treatments for asthma are available; however, they are frequently associated with adverse effects such as growth retardation, neurological disorders (e.g., catatonia, poor concentration, and insomnia), and physiological disorders (e.g., immunosuppression, hypertension, hyperglycemia, and osteoporosis). Methods: Korean Red Ginseng has long been used to treat numerous diseases in many countries, and we investigated the anti-asthmatic effects and mechanisms of action of Korean Red Ginseng. Eighty-four BALB/c mice were assigned to 6 treatment groups: control, ovalbumin-induced asthma group, dexamethasone treatment group, and 3 groups treated with Korean Red Ginseng water extract (KRGWE) at 5, 25, or 50 mg/kg/day for 5 days. Anti-asthmatic effects of KRGWE were assessed based on biological changes, such as white blood cell counts and differential counts in the bronchoalveolar lavage fluid, serum IgE levels, and histopathological changes in the lungs, and by examining anti-asthmatic mechanisms, such as the cytokines associated with Th1, Th2, and Treg cells and inflammation pathways. Results: KRGWE affected ovalbumin-induced changes, such as increased white blood cell counts, increased IgE levels, and morphological changes (mucous hypersecretion, epithelial cell hyperplasia, inflammatory cell infiltration) by downregulating cytokines such as IL-12, IL-4, and IL-6 via GATA-3 inactivation and suppression of inflammation via NF-kB/COX-2 and PGE2 pathways. Conclusion: KRGWE is a promising drug for asthma treatment.  2020 The Korean Society of Ginseng. Publishing services by Elsevier B.V. This is an open access article

涉及技术：K1-Fluo 激光荧光共聚焦技术

关键词：asthma

5.      K284-6111 alleviates memory impairment and neuroinflammation in Tg2576 mice by inhibition of Chitinase-3-like 1 regulating ERK-dependent PTX3 pathway

Hyeon Joo Ham, Yong Sun Lee, Jaesuk Yun, Dong Ju Son, Hee Pom Lee, Sang-Bae Han and Jin Tae Hong

摘要：

Background: Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders characterized by gradual memory loss and neuropsychiatric symptoms. We have previously demonstrated that the 2-({3-[2-(1- cyclohexene-1-yl)ethyl]-6,7-dimethoxy-4-oxo-3,4-dihydro-2-quinazolinyl}sulfanyl)-N-(4-ethylphenyl)but* (K284- 6111), the inhibitor of CHI3L1, has the inhibitory effect on memory impairment in Αβ infusion mouse model and on LPS-induced neuroinflammation in the murine BV-2 microglia and primary cultured astrocyte. Methods: In the present study, we investigated the inhibitory effect of K284-6111 on memory dysfunction and neuroinflammation in Tg2576 transgenic mice, and a more detailed correlation of CHI3L1 and AD. To investigate the effects of K284-6111 on memory dysfunction, we administered K284-6111 (3 mg/kg, p.o.) daily for 4 weeks to Tg2576 mice, followed by behavioral tests of water maze test, probe test, and passive avoidance test. Results: Administration of K284-6111 alleviated memory impairment in Tg2576 mice and had the effect of reducing the accumulation of Aβ and neuroinflammatory responses in the mouse brain. K284-6111 treatment also selectively inactivated ERK and NF-κB pathways, which were activated when CHI3L1 was overexpressed, in the mouse brain and in BV-2 cells. Web-based gene network analysis and our results of gene expression level in BV-2 cells showed that CHI3L1 is closely correlated with PTX3. Our result revealed that knockdown of PTX3 has an inhibitory effect on the production of inflammatory proteins and cytokines, and on the phosphorylation of ERK and IκBα. Conclusion: These results suggest that K284-6111 could improve memory dysfunction by alleviating neuroinflammation through inhibiting CHI3L1 enhancing ERK-dependent PTX3 pathway

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关键词：Alzheimer’s disease, Neuroinflammation, CHI3L1, ERK, NF-κB

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