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Inhibition of Ca2+-calpain signaling is a new mechanism using Laminaria japonica polysaccharide to prevent macrophage foam cell formation and atherosclerosis

文献类型： 外文期刊

作者： Li, Xue-Ying 1 ; Kuang, Dan-Dan 1 ; Guo, An-Jun 1 ; Deng, Yuan-Yuan 4 ; Pan, Li-Hua 1 ; Li, Qiang-Ming 1 ; Luo, Jian-Ping 1 ; Zha, Xue-Qiang 1 ;

作者机构： 1.Hefei Univ Technol, Engn Res Ctr Bioproc, Minist Educ, 193 Tunxi Rd, Hefei 230009, Peoples R China

2.Hefei Univ Technol, Sch Food & Biol Engn, 193 Tunxi Rd, Hefei 230009, Peoples R China

3.Hefei Univ Technol, Key Lab Metab & Regulat Major Dis Anhui Higher Edu, 193 Tunxi Rd, Hefei 230009, Peoples R China

4.Guangdong Acad Agr Sci, Sericultural & Agrifood Res Inst, Guangzhou 510610, Peoples R China

5.Minist Agr & Rural Affairs, Key Lab Funct Foods, Guangzhou 510610, Peoples R China

6.Guangdong Key Lab Agr Prod Proc, Guangzhou 510610, Peoples R China

期刊名称：FOOD & FUNCTION （ 影响因子：6.1； 五年影响因子：6.5 ）

ISSN： 2042-6496

年卷期： 2023 年 14 卷 9 期

页码：

收录情况： SCI

摘要： The Ca2+-calpain signaling plays a pivotal role in regulating the upstream signaling pathway of cellular autophagy. The aim of the current work was to investigate the role of Ca2+-calpain signaling in the regulation of macrophage autophagy by a Laminaria japonica polysaccharide (LJP61A) in Ox-LDL induced macrophages and high fat diet fed atherosclerotic mice. Results revealed that the LJP61A markedly decreased the levels of intracellular Ca2+, calpain1, calpain2 and their downstream effectors (Gsa, cAMP and IP3), and simultaneously enhanced autophagy activity and lipid metabolism, thereby reducing lipid accumulation in the Ox-LDL stimulated macrophages and lipid-laden plaques in atherosclerotic mice. Moreover, BAPTA-AM (a Ca2+ chelator) and calpeptin (a calpain inhibitor) synergistically strengthened the beneficial effects of LJP61A on autophagy and lipid metabolism by decreasing the levels of intracellular Ca2+, calpain1, calpain2, and their downstream effectors (Gsa, cAMP and IP3) induced by Ox-LDL. These findings suggested that the LJP61A suppressed macrophage derived foam cell formation and atherosclerosis by modulating the Ca2+-calpain-mediated autophagy.

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