Kaixuan Qibi granules attenuate myocardial fibrosis through BRD4 blockade regulated by the NF-κB/NLRP3 signaling pathway.
OpenAlex 토픽 ·
Cardiac Fibrosis and Remodeling
Signaling Pathways in Disease
Microbial Metabolism and Applications
[BACKGROUND AND AIM] Kaixuan Qibi granules (KXGs) have exhibited favorable therapeutic outcomes in addressing a wide range of ailments.
APA
Rui Huang, Gang Luo, et al. (2026). Kaixuan Qibi granules attenuate myocardial fibrosis through BRD4 blockade regulated by the NF-κB/NLRP3 signaling pathway.. Journal of traditional and complementary medicine, 16(3), 271-283. https://doi.org/10.1016/j.jtcme.2025.03.001
MLA
Rui Huang, et al.. "Kaixuan Qibi granules attenuate myocardial fibrosis through BRD4 blockade regulated by the NF-κB/NLRP3 signaling pathway.." Journal of traditional and complementary medicine, vol. 16, no. 3, 2026, pp. 271-283.
PMID
42006487
Abstract
[BACKGROUND AND AIM] Kaixuan Qibi granules (KXGs) have exhibited favorable therapeutic outcomes in addressing a wide range of ailments. They have established their efficacy as a traditional Chinese medicine formulation, particularly for cardiovascular and cerebrovascular diseases associated with myocardial fibrosis (MF). Targeting of bromodomain-containing protein 4 (BRD4) represents an efficacious strategy for addressing inflammation (a pivotal factor in MF progression). However, revealing the inhibitory impact of KXGs on BRD4 in MF development is elusive. We investigated the impact of KXGs on MF and elucidated the regulatory mechanism of BRD4 in MF by KXGs and .
[EXPERIMENTAL PROCEDURE] Induction of an model of MF was achieved in C57BL/6 mice by intraperitoneal administration of isoproterenol (ISO) over 21 days. After administering different doses of KXGs and fosinopril (FOS) via oral gavage for 21 days, metabolite levels, myofibril accumulation, and collagen deposition were assessed using standardized assays. To simulate an inflammatory reaction , mouse monocyte-macrophage leukemia (RAW264.7) cells were stimulated with lipopolysaccharide (LPS). The intervention effect of KXGs on BRD4 and the nuclear factor-kappa B/NOD-like receptor protein 3 (NF-κB/NLRP3) pathway was evaluated using western blotting and immunofluorescence methods.
[RESULTS] In this study, we observed a notable reduction in the extent of fibrotic tissue accompanied by organized collagen following treatment with KXGs. KXGs exhibited a significant regulatory effect on metabolite levels while also inhibiting BRD4-related pathways and the inflammatory response. Later, KXGs exhibited downregulation the expression of BRD4, phosphorylated (p)-NF-κB p65 (phosphor/total), NLRP3, ASC, caspase-1, and interleukin-1β (IL-1β) in both models of MF development.
[CONCLUSION] KXGs attenuated MF progression by modulating the NF-κB/NLRP3 signaling pathway through inhibition of BRD4 activity.
[EXPERIMENTAL PROCEDURE] Induction of an model of MF was achieved in C57BL/6 mice by intraperitoneal administration of isoproterenol (ISO) over 21 days. After administering different doses of KXGs and fosinopril (FOS) via oral gavage for 21 days, metabolite levels, myofibril accumulation, and collagen deposition were assessed using standardized assays. To simulate an inflammatory reaction , mouse monocyte-macrophage leukemia (RAW264.7) cells were stimulated with lipopolysaccharide (LPS). The intervention effect of KXGs on BRD4 and the nuclear factor-kappa B/NOD-like receptor protein 3 (NF-κB/NLRP3) pathway was evaluated using western blotting and immunofluorescence methods.
[RESULTS] In this study, we observed a notable reduction in the extent of fibrotic tissue accompanied by organized collagen following treatment with KXGs. KXGs exhibited a significant regulatory effect on metabolite levels while also inhibiting BRD4-related pathways and the inflammatory response. Later, KXGs exhibited downregulation the expression of BRD4, phosphorylated (p)-NF-κB p65 (phosphor/total), NLRP3, ASC, caspase-1, and interleukin-1β (IL-1β) in both models of MF development.
[CONCLUSION] KXGs attenuated MF progression by modulating the NF-κB/NLRP3 signaling pathway through inhibition of BRD4 activity.
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