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Войти в исследования Canadian journal of diabetes · 2026
Glaucocalyxin B Attenuates Diabetic Cardiomyopathy by Suppressing the NLRP3 Inflammasome and Restoring Gut Microbiota Homeostasis.
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Zhang Xinxin, Wu Jingping
Аннотация
OBJECTIVES: Glaucocalyxin B (GLB) has documented anti-inflammatory activity in several disease contexts; however, its role in diabetic cardiomyopathy (DCM)-associated inflammatory injury remains insufficiently defined. In this study we aimed to evaluate whether GLB alleviates myocardial inflammation and injury in DCM and to explore the underlying mechanisms.
METHODS: We combined network pharmacology with experimental validation using a streptozotocin-induced diabetic rat model (8-week protocol) and high-glucose-challenged H9c2 rat cardiomyocytes. Oxidative stress-related indices (e.g. reactive oxygen species [ROS] and malondialdehyde [MDA]) and antioxidant capacity were assessed in vivo and in vitro. Gut microbiota composition was profiled by 16S rRNA sequencing. Activation of inflammatory signalling was evaluated with a focus on the nuclear factor-kappaB/NOD-like receptor pyrin domain-containing 3 (NFκB/NLRP3) axis.
RESULTS: Network pharmacology suggested that GLB targets were enriched in pathways related to cardiomyocyte regulation and DCM-associated processes, including inflammation, apoptosis, and oxidative stress responses. In both diabetic rat myocardium and high-glucose-treated H9c2 cells, GLB reduced oxidative stress burden, as evidenced by decreased ROS and MDA levels and improved antioxidant-related readouts. In addition, GLB was associated with increased gut microbial richness and diversity in diabetic rats. Mechanistically, GLB treatment was accompanied by suppression of NFκB/NLRP3 pathway activation, consistent with attenuation of inflammatory injury.
CONCLUSIONS: These findings provide initial evidence that GLB mitigates oxidative stress and inflammatory damage in DCM. The cardioprotective effects of GLB appear to involve modulation of the NFκB/NLRP3 signalling pathway and partial restoration of gut microbial diversity, supporting GLB as a promising candidate for further investigation in DCM.
METHODS: We combined network pharmacology with experimental validation using a streptozotocin-induced diabetic rat model (8-week protocol) and high-glucose-challenged H9c2 rat cardiomyocytes. Oxidative stress-related indices (e.g. reactive oxygen species [ROS] and malondialdehyde [MDA]) and antioxidant capacity were assessed in vivo and in vitro. Gut microbiota composition was profiled by 16S rRNA sequencing. Activation of inflammatory signalling was evaluated with a focus on the nuclear factor-kappaB/NOD-like receptor pyrin domain-containing 3 (NFκB/NLRP3) axis.
RESULTS: Network pharmacology suggested that GLB targets were enriched in pathways related to cardiomyocyte regulation and DCM-associated processes, including inflammation, apoptosis, and oxidative stress responses. In both diabetic rat myocardium and high-glucose-treated H9c2 cells, GLB reduced oxidative stress burden, as evidenced by decreased ROS and MDA levels and improved antioxidant-related readouts. In addition, GLB was associated with increased gut microbial richness and diversity in diabetic rats. Mechanistically, GLB treatment was accompanied by suppression of NFκB/NLRP3 pathway activation, consistent with attenuation of inflammatory injury.
CONCLUSIONS: These findings provide initial evidence that GLB mitigates oxidative stress and inflammatory damage in DCM. The cardioprotective effects of GLB appear to involve modulation of the NFκB/NLRP3 signalling pathway and partial restoration of gut microbial diversity, supporting GLB as a promising candidate for further investigation in DCM.