Journal of ethnopharmacology · 2025
(2S)-5-methoxy-6-methyl-flavan-7-ol from Sanguis draconis attenuates atherosclerosis in ApoE-/- mice by inhibiting monocyte-endothelial cell adhesion.
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Wang Xinyu, Zhao Maoyuan, Xue Weigang, Wang Junjiao, Pang Xueping, Zheng Deli, Zhang Ruijie, Huo Huixia, Huang Yangli, Sun Panxi, Tu Pengfei, Zheng Jiao, Li Jun
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Sanguis draconis act traditional Chinese medicine has now been used clinically for the treatment of cardiovascular diseases, and the polyphenol are recognized as their main active ingredients.
AIM OF THE STUDY: Given that flavonoids have been identified as the primary active ingredients of Sanguis draconis, this research intends to explore the anti-atherosclerotic effect and underlying mechanism of action of (2S)-5-methoxy-6-methyl-flavan-7-ol (XJ8) in Sanguis draconis.
MATERIALS AND METHODS: Atherosclerosis was induced in the aortic sinus of ApoE-/- mice via a high-fat diet, and the protective efficacy of XJ8 against atherosclerosis was examined. Network pharmacology was used to explore the potential target of XJ8 in the treatment of atherosclerosis. An endothelial cell model was established using nitric oxide (NO) to initiate cellular inflammatory responses and monocyte-endothelial cell adhesion, wherein the effects and the underlying mechanism of XJ8 on cellular adhesion were observed.
RESULTS: This study demonstrated that XJ8 attenuated the atherosclerotic burden in the aortic sinus of the high-fat diet-induced ApoE-/- mice, concurrently reducing body fat levels. Network pharmacology analysis identified potential targets of action of XJ8, predominantly involving inflammatory pathways. Subsequent investigations revealed that XJ8 treatment remarkably suppressed NO-induced monocyte-endothelial cell adhesion by downregulating intercellular adhesion molecule-1 (ICAM-1) expression. Mechanistically, XJ8 inhibited the NO-induced endothelial inflammation through the regulation of JNK/Stat3 and NF-κB/IκBα pathways.
CONCLUSION: This study demonstrates that XJ8 inhibits intercellular adhesion by downregulating ICAM-1 expression through the NF-κB/IκBα and JNK/Stat3 signaling pathways, thereby ameliorating atherosclerosis. These mechanistic insights offer novel therapeutic strategies for clinical atherosclerosis management.
AIM OF THE STUDY: Given that flavonoids have been identified as the primary active ingredients of Sanguis draconis, this research intends to explore the anti-atherosclerotic effect and underlying mechanism of action of (2S)-5-methoxy-6-methyl-flavan-7-ol (XJ8) in Sanguis draconis.
MATERIALS AND METHODS: Atherosclerosis was induced in the aortic sinus of ApoE-/- mice via a high-fat diet, and the protective efficacy of XJ8 against atherosclerosis was examined. Network pharmacology was used to explore the potential target of XJ8 in the treatment of atherosclerosis. An endothelial cell model was established using nitric oxide (NO) to initiate cellular inflammatory responses and monocyte-endothelial cell adhesion, wherein the effects and the underlying mechanism of XJ8 on cellular adhesion were observed.
RESULTS: This study demonstrated that XJ8 attenuated the atherosclerotic burden in the aortic sinus of the high-fat diet-induced ApoE-/- mice, concurrently reducing body fat levels. Network pharmacology analysis identified potential targets of action of XJ8, predominantly involving inflammatory pathways. Subsequent investigations revealed that XJ8 treatment remarkably suppressed NO-induced monocyte-endothelial cell adhesion by downregulating intercellular adhesion molecule-1 (ICAM-1) expression. Mechanistically, XJ8 inhibited the NO-induced endothelial inflammation through the regulation of JNK/Stat3 and NF-κB/IκBα pathways.
CONCLUSION: This study demonstrates that XJ8 inhibits intercellular adhesion by downregulating ICAM-1 expression through the NF-κB/IκBα and JNK/Stat3 signaling pathways, thereby ameliorating atherosclerosis. These mechanistic insights offer novel therapeutic strategies for clinical atherosclerosis management.