Co-administrating apigenin in a high-cholesterol diet prevents hypercholesterolaemia in golden hamsters

Wong, Tak‐Lam; Tan, Yan Qin; Lin, Shumei; Leung, Lai K.

doi:10.1111/jphp.12953

Cited by 8 publications

(6 citation statements)

References 36 publications

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“…In another study by Wong et al, apigenin (60 and 300 ppm) was co-administered with a high-cholesterol diet in golden hamsters. Consistent with the findings of the previous study, hamsters fed with apigenin showcased a decrease in serum total cholesterol and triglyceride levels [ 23 ]. Apigenin co-administered with the diet resulted in a protective effect against aortic plaque formation and promoted the fecal elimination of cholesterol.…”

Section: Therapeutic Potential Of Apigenin In Cardiovascular Disorderssupporting

confidence: 91%

Pharmacological and Molecular Insight on the Cardioprotective Role of Apigenin

Thomas

Jha

et al. 2023

Nutrients

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Apigenin is a naturally occurring dietary flavonoid found abundantly in fruits and vegetables. It possesses a wide range of biological properties that exert antioxidant, anti-inflammatory, anticancer, and antibacterial effects. These effects have been reported to be beneficial in the treatment of atherosclerosis, stroke, hypertension, ischemia/reperfusion-induced myocardial injury, and diabetic cardiomyopathy, and provide protection against drug-induced cardiotoxicity. These potential therapeutic effects advocate the exploration of the cardioprotective actions of apigenin. This review focuses on apigenin, and the possible pharmacological mechanisms involved in the protection against cardiovascular diseases. We further discuss its therapeutic uses and highlight its potential applications in the treatment of various cardiovascular disorders. Apigenin displays encouraging results, which may have implications in the development of novel strategies for the treatment of cardiovascular diseases. With the commercial availability of apigenin as a dietary supplement, the outcomes of preclinical studies may provide the investigational basis for future translational strategies evaluating the potential of apigenin in the treatment of cardiovascular disorders. Further preclinical and clinical investigations are required to characterize the safety and efficacy of apigenin and establish it as a nutraceutical as well as a therapeutic agent to be used alone or as an adjuvant with current drugs.

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Section: Therapeutic Potential Of Apigenin In Cardiovascular Disorderssupporting

confidence: 91%

Pharmacological and Molecular Insight on the Cardioprotective Role of Apigenin

Thomas

Jha

et al. 2023

Nutrients

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“…Various flavonoids have been reported to attenuate the progression of atherosclerosis. Wong et al (2018) showed that API ameliorates hyperlipidemia, a risk factor for atherosclerosis, by reducing cholesterol biosynthesis. Disturbed lipid metabolism in macrophages and foam cell formation are key factors promoting the progression of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Apigenin inhibits macrophage pyroptosis through regulation of oxidative stress and the NF‐κB pathway and ameliorates atherosclerosis

Weng

Luo

Dai

et al. 2023

Phytotherapy Research

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Pyroptosis plays an important role in inflammatory diseases such as viral hepatitis and atherosclerosis. Apigenin exhibits various bioactivities, particularly anti‐inflammation, but its effect on pyroptosis remains unclear. The aim of this study is to investigate the effect of apigenin on pyroptosis and explore its potential against inflammatory diseases. THP‐1 macrophages treated by lipopolysaccharides/adenosine 5′‐triphosphate were used as the in vitro pyroptosis model. Western blot was used to detect the expression of NLRP3 inflammasome components and key regulators. Immunofluorescence was used to observe ROS production and intracellular location of p65. The potential of apigenin against inflammatory diseases was evaluated using atherosclerotic mice. Plaque progression was observed by pathological staining. Immunofluorescence was used to observe the expression of NLRP3 inflammasome components in plaques. The results showed that apigenin inhibited NLRP3 inflammasome activation. Apigenin reduced ROS overproduction and inhibited p65 nuclear translocation. Additionally, apigenin decreased the expression of NLRP3 inflammasome components in the plaque. Plaque progression was inhibited by apigenin. In conclusion, apigenin exhibited a preventive effect on macrophage pyroptosis by reducing oxidative stress and inhibiting the NF‐κB pathway. Apigenin may alleviate atherosclerosis at least partially by inhibiting macrophage pyroptosis. These findings suggest apigenin to be a promising therapeutic agent for inflammatory diseases.

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“…Combination index (CI) analysis was performed using the Chou-Talalay method. Western blot analysis was performed as previously described [ 77 , 78 ] using the antibodies tabulated in SI 22 . All functional assays were performed in a medium with 2% FBS.…”

Section: Methodsmentioning

confidence: 99%

Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma

Tan,

Sun,

Zhang

et al. 2024

Cell Death Dis

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Therapeutic targeting of KRAS-mutant pancreatic ductal adenocarcinoma (PDAC) has remained a significant challenge in clinical oncology. Direct targeting of KRAS has proven difficult, and inhibition of the KRAS effectors have shown limited success due to compensatory activation of survival pathways. Being a core downstream effector of the KRAS-driven p44/42 MAPK and PI3K/AKT pathways governing intrinsic apoptosis, BAD phosphorylation emerges as a promising therapeutic target. Herein, a positive association of the pBADS99/BAD ratio with higher disease stage and worse overall survival of PDAC was observed. Homology-directed repair of BAD to BADS99A or small molecule inhibition of BADS99 phosphorylation by NCK significantly reduced PDAC cell viability by promoting cell cycle arrest and apoptosis. NCK also abrogated the growth of preformed colonies of PDAC cells in 3D culture. Furthermore, high-throughput screening with an oncology drug library to identify potential combinations revealed a strong synergistic effect between NCK and MEK inhibitors in PDAC cells harboring either wild-type or mutant-KRAS. Mechanistically, both mutant-KRAS and MEK inhibition increased the phosphorylation of BADS99 in PDAC cells, an effect abrogated by NCK. Combined pBADS99-MEK inhibition demonstrated strong synergy in reducing cell viability, enhancing apoptosis, and achieving xenograft stasis in KRAS-mutant PDAC. In conclusion, the inhibition of BADS99 phosphorylation enhances the efficacy of MEK inhibition, and their combined inhibition represents a mechanistically based and potentially effective therapeutic strategy for the treatment of KRAS-mutant PDAC.

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Co-administrating apigenin in a high-cholesterol diet prevents hypercholesterolaemia in golden hamsters

Abstract: This study illustrated that dietary administration of apigenin attenuated HC feeding-induced hypercholesterolemia in hamsters.

Cited by 8 publications

References 36 publications

Pharmacological and Molecular Insight on the Cardioprotective Role of Apigenin

Pharmacological and Molecular Insight on the Cardioprotective Role of Apigenin

Apigenin inhibits macrophage pyroptosis through regulation of oxidative stress and the NF‐κB pathway and ameliorates atherosclerosis

Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma

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