Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Baicalin and ginsenoside Rb1 suppress the activation of cardiac fibroblasts via regulating the GRK2/AT1R/MasR network.
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Zhang Honglei, Xu Jiaxing, Li Wenting, Wang Ziqing, Wang Zhuqi, Liu Kang
Аннотация
BACKGROUND: Obesity is a risk factor for cardiovascular diseases. Baicalin and ginsenoside Rb1 are the main components of the Scutellariae Radix-Ginseng Radix et Rhizoma herb pair. However, the effects on obesity-related cardiac fibrosis remain unclear.
PURPOSE: To evaluate the effects of baicalin, Rb1, and their combination on cardiac fibroblast (CF) activation in the background of obesity.
METHODS: The CFs were incubated with the conditioned medium derived from the visceral adipose tissue (T-CM) and angiotensin II (Ang II), and the high-fat diet (HFD)-fed mice received transverse aortic constriction (TAC) to induce pressure overload-mediated cardiac fibrosis.
RESULTS: Co-stimulation of T-CM and Ang II triggered a rippled change in the protein expression of GRK2, Ang II type 1 receptor (AT1R), and Ang 1-7 receptor Mas (MasR), leading to the activation of CFs, evidenced by the upregulation of α-SMA, TGF-β1, and Col-1. Baicalin, Rb1, combined treatment, and paroxetine decreased HFD-induced insulin resistance, reduced the upregulation of GRK2, and counterpoised the Ang II/AT1R and Ang 1-7/MasR axis, thereby suppressing CF activation and ameliorating cardiac fibrosis and cardiac function. The component combination showed a more potent effect. Inhibiting the phosphorylation of NF-κB and STAT3 through GRK2 downregulation contributed to the effect of baicalin and Rb1 on AT1R and MasR.
CONCLUSION: Baicalin, Rb1, and their combination suppress the CF activation and cardiac fibrosis in the background of obesity by regulating the expressions and activities of the GRK2/AT1R/MasR network. The finding might extend the understanding of their multifaceted effects and expand their potential applications.
PURPOSE: To evaluate the effects of baicalin, Rb1, and their combination on cardiac fibroblast (CF) activation in the background of obesity.
METHODS: The CFs were incubated with the conditioned medium derived from the visceral adipose tissue (T-CM) and angiotensin II (Ang II), and the high-fat diet (HFD)-fed mice received transverse aortic constriction (TAC) to induce pressure overload-mediated cardiac fibrosis.
RESULTS: Co-stimulation of T-CM and Ang II triggered a rippled change in the protein expression of GRK2, Ang II type 1 receptor (AT1R), and Ang 1-7 receptor Mas (MasR), leading to the activation of CFs, evidenced by the upregulation of α-SMA, TGF-β1, and Col-1. Baicalin, Rb1, combined treatment, and paroxetine decreased HFD-induced insulin resistance, reduced the upregulation of GRK2, and counterpoised the Ang II/AT1R and Ang 1-7/MasR axis, thereby suppressing CF activation and ameliorating cardiac fibrosis and cardiac function. The component combination showed a more potent effect. Inhibiting the phosphorylation of NF-κB and STAT3 through GRK2 downregulation contributed to the effect of baicalin and Rb1 on AT1R and MasR.
CONCLUSION: Baicalin, Rb1, and their combination suppress the CF activation and cardiac fibrosis in the background of obesity by regulating the expressions and activities of the GRK2/AT1R/MasR network. The finding might extend the understanding of their multifaceted effects and expand their potential applications.