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没食子酸表没食子儿茶素酯通过 有效影响 3T3-L1 前体脂肪细胞衰老和抗 SASP 作用,优于其他生物活性物质。

Epigallocatechin Gallate Effectively Affects Senescence and Anti-SASP via in 3T3-L1 Preadipocytes in Comparison with Other Bioactive Substances.

机构信息

Department of Nutritional Sciences, University of Vienna, 1090 Vienna, Austria.

HealthBioCare GmbH Nußdorferstraße 67, 1090 Wien, Austria.

出版信息

Oxid Med Cell Longev. 2020 Oct 21;2020:4793125. doi: 10.1155/2020/4793125. eCollection 2020.

DOI:10.1155/2020/4793125
PMID:33149809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7603628/
Abstract

AIM

We investigated different bioactive compounds including epigallocatechin gallate (EGCG), anthocyanidin, resveratrol, phloretin, spermidine, butyrate, and -hydroxybutyrate with regard to their effect on via and modulation of the proinflammatory senescence-associated secretory phenotype (SASP) in senescence induced 3T3-L1 preadipocytes.

METHODS

For induction of senescence, 3T3-L1 preadipocytes were incubated with bromodeoxyuridine (BrdU) for 8 days. Cell cycle inhibition was observed, and -galactosidase activity was measured. After BrdU treatment, cells were treated with different bioactive compounds in various concentrations for 96 h. ELISA was used for determining proinflammatory cytokine IL6 in SASP cells.

RESULTS

increased significantly after BrdU incubation compared to untreated control ( < 0.01). All secondary plant ingredients used for treatment, but not anthocyanidin 50 M, decrease expression ( < 0.05), whereas most endogenous substances did not attenuate . IL6 secretion positively correlated with ( < 0.01), whereas EGCG could diminish both, IL6 and with the strongest effect ( < 0.01). Although positively correlated with activation ( < 0.05), only resveratrol ( < 0.01) and anthocyanidin ( < 0.05) could activate significantly. Solely anthocyanidin 50 M ( < 0.05) and 100 M ( < 0.01) and EGCG 50 M ( < 0.01) could increase expression. Activation of with EGCG correlated with lowered IL6 secretion significantly ( < 0.05) but not with anthocyanidin.

CONCLUSION

Accumulation of senescent cells in adipose tissue plays an important role in obesity and age-related diseases. , located in the mitochondria, can regulate ROS via different pathways. Thus, targeting activating compounds such as EGCG may delay senescence of cells and senescence induced inflammatory processes.

摘要

目的

我们研究了不同的生物活性化合物,包括表没食子儿茶素没食子酸酯(EGCG)、花青素、白藜芦醇、根皮苷、亚精胺、丁酸盐和β-羟基丁酸,探讨它们对衰老诱导的 3T3-L1 前脂肪细胞中通过炎性衰老相关分泌表型(SASP)的促炎作用和调节作用。

方法

为了诱导衰老,将 3T3-L1 前脂肪细胞用溴脱氧尿苷(BrdU)孵育 8 天。观察细胞周期抑制情况,并测定β-半乳糖苷酶活性。BrdU 处理后,用不同浓度的各种生物活性化合物处理细胞 96 小时。用 ELISA 法测定 SASP 细胞中促炎细胞因子 IL6。

结果

与未处理对照组相比,BrdU 孵育后 表达显著增加(<0.01)。所有用于治疗的植物次生成分,除 50μM 花青素外,均能降低 表达(<0.05),而大多数内源性物质则不能减弱 表达。IL6 分泌与 呈正相关(<0.01),而 EGCG 则能显著降低 IL6 和 (<0.01)。虽然 与 激活呈正相关(<0.05),但只有白藜芦醇(<0.01)和花青素(<0.05)能显著激活 。只有花青素 50μM(<0.05)和 100μM(<0.01)和 EGCG 50μM(<0.01)能增加 表达。EGCG 激活 与 IL6 分泌降低显著相关(<0.05),但与花青素无关。

结论

脂肪组织中衰老细胞的积累在肥胖和与年龄相关的疾病中起着重要作用。 位于线粒体中,可以通过不同的途径调节 ROS。因此,靶向 激活化合物,如 EGCG,可能会延缓细胞衰老和衰老诱导的炎症过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/5f8c6c771b50/OMCL2020-4793125.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/04ff6c5678e5/OMCL2020-4793125.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/bf076e027073/OMCL2020-4793125.005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/2b2804610964/OMCL2020-4793125.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/5f8c6c771b50/OMCL2020-4793125.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/04ff6c5678e5/OMCL2020-4793125.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/00af9ed73bbf/OMCL2020-4793125.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/2fc8360f2938/OMCL2020-4793125.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/9201f6b3abe7/OMCL2020-4793125.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/bf076e027073/OMCL2020-4793125.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/754fa7ff40fa/OMCL2020-4793125.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/2b2804610964/OMCL2020-4793125.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44c5/7603628/5f8c6c771b50/OMCL2020-4793125.008.jpg

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