Anti-diabetic effects of Grifola frondosa bioactive compound and its related molecular signaling pathways in palmitate-induced C2C12 cells

Wu, Shu-Jing; Tung, Yi-Jou; Ng, Lean‐Teik

doi:10.1016/j.jep.2020.112962

Cited by 18 publications

(4 citation statements)

References 37 publications

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“…Our study has a few limitations. Although we confirmed the anti-diabetic effect of QG in C2C12 muscles, a common in vitro model for such studies [50,51], it would be valuable to assess the influence of QG on lipid buildup or differentiation in 3T3-L1 adipocytes, considering the association of T2DM treatments with obesity [36,52]. In addition, various intermediate molecular markers, such as AS160, GLUT-4, and DAG, could be used to further support our study.…”

Section: Discussionsupporting

confidence: 64%

Exploring the Anti-Diabetic Potential of Quercetagitrin through Dual Inhibition of PTPN6 and PTPN9

Gone,

Go,

Nam

et al. 2024

Nutrients

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Protein tyrosine phosphatases (PTPs) are pivotal contributors to the development of type 2 diabetes (T2DM). Hence, directing interventions towards PTPs emerges as a valuable therapeutic approach for managing type 2 diabetes. In particular, PTPN6 and PTPN9 are targets for anti-diabetic effects. Through high-throughput drug screening, quercetagitrin (QG) was recognized as a dual-target inhibitor of PTPN6 and PTPN9. We observed that QG suppressed the catalytic activity of PTPN6 (IC50 = 1 μM) and PTPN9 (IC50 = 1.7 μM) in vitro and enhanced glucose uptake by mature C2C12 myoblasts. Additionally, QG increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and insulin-dependent phosphorylation of Akt in mature C2C12 myoblasts. It further promoted the phosphorylation of Akt in the presence of palmitic acid, suggesting the attenuation of insulin resistance. In summary, our results indicate QG’s role as a potent inhibitor targeting both PTPN6 and PTPN9, showcasing its potential as a promising treatment avenue for T2DM.

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Section: Discussionsupporting

confidence: 64%

Exploring the Anti-Diabetic Potential of Quercetagitrin through Dual Inhibition of PTPN6 and PTPN9

Gone,

Go,

Nam

et al. 2024

Nutrients

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“…Other studies have shown that the upregulation of JNK phosphorylation can promote the expression of MAFbx and induce muscle atrophy and cell death [ 69 – 71 ]. Therefore, inhibition of JNK phosphorylation can play a protective role: curcumin reduces the inflammatory damage of skeletal muscle cells by inhibiting the JNK/NF- κ B pathway [ 72 ], and Grifola frondosa promotes glucose uptake and growth of C2C12 myotube cells by downregulating JNK phosphorylation [ 73 ]. These results show that promoting ERK phosphorylation and inhibiting JNK phosphorylation can protect muscle tissue and C2C12 myotube cells.…”

Section: Discussionmentioning

confidence: 99%

Silibinin Alleviates Muscle Atrophy Caused by Oxidative Stress Induced by Cisplatin through ERK/FoxO and JNK/FoxO Pathways

Chi

Zhang

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Cisplatin (DDP), a widely used chemotherapeutic drug in cancer treatment, causes oxidative stress, resulting in cancer cachexia and skeletal muscle atrophy. This study investigated the effects and activity of silibinin (SLI) in reducing DDP-induced oxidative stress and skeletal muscle atrophy in vivo and in vitro. SLI alleviated weight loss, food intake, muscle wasting, adipose tissue depletion, and organ weight reduction induced by DDP and improved the reduction of grip force caused by DDP. SLI can attenuated the increase in reactive oxygen species (ROS) levels, the decrease in Nrf2 expression, the decrease in the fiber cross-sectional area, and changes in fiber type induced by DDP. SLI regulated the ERK/FoxO and JNK/FoxO pathways by downregulating the abnormal increase in ROS and Nrf2 expression in DDP-treated skeletal muscle and C2C12 myotube cells. Further, SLI inhibited the upregulation of MAFbx and Mstn, the downregulation of MyHC and MyoG, the increase in protein degradation, and the decrease of protein synthesis. The protective effects of SLI were reversed by cotreatment with JNK agonists and ERK inhibitors. These results suggest that SLI can reduce DDP-induced skeletal muscle atrophy by reducing oxidative stress and regulating ERK/FoxO and JNK/FoxO pathways.

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“…Ng et al reported the antidiabetic effect of 21a that was due to the upregulation of glucose absorption and modulation of the PI3K/Akt, MAPK, and GLUT-4 signaling pathways [ 161 ].…”

Section: Endoperoxidesmentioning

confidence: 99%

Structure and Biological Activity of Ergostane-Type Steroids from Fungi

2022

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Mushrooms are known not only for their taste but also for beneficial effects on health attributed to plethora of constituents. All mushrooms belong to the kingdom of fungi, which also includes yeasts and molds. Each year, hundreds of new metabolites of the main fungal sterol, ergosterol, are isolated from fungal sources. As a rule, further testing is carried out for their biological effects, and many of the isolated compounds exhibit one or another activity. This study aims to review recent literature (mainly over the past 10 years, selected older works are discussed for consistency purposes) on the structures and bioactivities of fungal metabolites of ergosterol. The review is not exhaustive in its coverage of structures found in fungi. Rather, it focuses solely on discussing compounds that have shown some biological activity with potential pharmacological utility.

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Anti-diabetic effects of Grifola frondosa bioactive compound and its related molecular signaling pathways in palmitate-induced C2C12 cells

Cited by 18 publications

References 37 publications

Exploring the Anti-Diabetic Potential of Quercetagitrin through Dual Inhibition of PTPN6 and PTPN9

Exploring the Anti-Diabetic Potential of Quercetagitrin through Dual Inhibition of PTPN6 and PTPN9

Silibinin Alleviates Muscle Atrophy Caused by Oxidative Stress Induced by Cisplatin through ERK/FoxO and JNK/FoxO Pathways

Structure and Biological Activity of Ergostane-Type Steroids from Fungi

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