Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca2+ related regulators

Zhu, Hua; Cao, Jianhong; Liang, Xiaofang; Luo, Meng; Wang, Anrong; Hu, Ling; Li, Ru-Liu

doi:10.1016/j.jgr.2022.05.010

Cited by 7 publications

(3 citation statements)

References 20 publications

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“…There are researches showed that knocking out the canonical transient receptor potential channel 1 (TRPC1) can decrease Ca + influx and ROS production, thereby exerting a protective effect on the heart. , The natural compound chlorogenic acid has been demonstrated to protect endothelial cells from LPC-induced injury by attenuating TRPC1 expression . Furthermore, the polysaccharides in Hedysarum Multijugum Maxim and Radix Salviae also exhibit inhibitory effects on TRPC1, , providing new directions for research in this field.…”

Section: Introductionmentioning

confidence: 99%

“… 4 , 5 The natural compound chlorogenic acid has been demonstrated to protect endothelial cells from LPC-induced injury by attenuating TRPC1 expression. 6 Furthermore, the polysaccharides in Hedysarum Multijugum Maxim and Radix Salviae also exhibit inhibitory effects on TRPC1, 7 , 8 providing new directions for research in this field.…”

Section: Introductionmentioning

confidence: 99%

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Exploring the Potential Mechanisms of Guanxinshutong Capsules in Treating Pathological Cardiac Hypertrophy based on Network Pharmacology, Computer-Aided Drug Design, and Animal Experiments

Liu,

Li,

Shao

et al. 2024

ACS Omega

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Cardiovascular diseases (CVDs) are significant causes of morbidity and mortality worldwide, and pathological cardiac hypertrophy (PCH) is an essential predictor of many heart diseases. Guanxinshutong capsule (GXST) is a Chinese patent medicine widely used in the clinical treatment of CVD, In our previous research, we identified 111 compounds of GXST. In order to reveal the potential molecular mechanisms by which GXST treats PCH, this study employed network pharmacology methods to screen for the active ingredients of GXST in treating PCH and predicted the potential targets. The results identified 26 active ingredients of GXST and 110 potential targets for PCH. Through a protein−protein interaction (PPI) network, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, we confirmed AKT1, MAPK1, and MAPK3 as the core proteins in GXST treatment of PCH, thus establishing the PI3K/ AKT and MAPK signaling pathways as the significant mechanisms of GXST in treating PCH. The results of molecular docking (MD) demonstrate that flavonoid naringenin and diterpenoid tanshinone iia have the highest binding affinity with the core protein.Before performing molecular dynamics simulations (MDSs), the geometric structure of naringenin and tanshinone iia was optimized using density functional theory (DFT) at the B97−3c level, and RESP2 atomic charge calculations were carried out at the B3LYP-D3(BJ)/def2-TZVP level. Further MDS results demonstrated that in the human body environment, the complex of naringenin and tanshinone iii with core proteins exhibited high stability, flexibility, and low binding free energy. Additionally, naringenin and tanshinone iia showed favorable absorption, distribution, metabolism, excretion, and toxicity (ADMET) characteristics and passed the drug similarity (DS) assessment. Ultrasound cardiograms and cardiac morphometric measurements in animal experiments demonstrate that GXST can improve the PCH induced by isoproterenol (ISO). Protein immunoblotting results indicate that GXST increases the expression of P-eNOS and eNOS by activating the PI3K/AKT signaling pathway and the MAPK signaling pathway, further elucidating the mechanism of action of GXST in treating PCH. This study contributes to the elucidation of the key ingredients and molecular mechanisms of GXST in treating PCH.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exploring the Potential Mechanisms of Guanxinshutong Capsules in Treating Pathological Cardiac Hypertrophy based on Network Pharmacology, Computer-Aided Drug Design, and Animal Experiments

Liu,

Li,

Shao

et al. 2024

ACS Omega

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“…Many hundreds of papers were published in the past year that use substances like aspirin, nonsteroidal anti-inflammatory drugs (indomethacin), or alcohol to damage the gastroduodenal mucosa and then highlight novel compounds to promote mucosal repair after injury. As an example, Panax ginseng effectively supported intestinal barrier recovery after indomethacin-induced injury by promoting the expression of transporters responsible for Ca 2+ -signaling [4 ▪ ], which is required for cell migration during restitution [5]. Likewise, a novel molecule that specifically targets focal adhesion kinase (FAK), M64HCl, was developed to activate FAK and promote wound healing, which also accelerated the repair of duodenal ulcers after treatment with indomethacin [6 ▪ ].…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology updates: gastroduodenal injury and repair mechanisms

Hagen

2023

Current Opinion in Gastroenterology

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Purpose of review Although the mucosal barrier serves as a primary interface between the environment and host, little is known about the repair of acute, superficial lesions or deeper, persistent lesions that if not healed, can be the site of increased permeability to luminal antigens, inflammation, and/or neoplasia development. Recent findings Recent studies on acute superficial lesions have focused on calcium signaling and focal adhesion kinase, which regulate cell migration and controlled matrix adhesion during restitution. Microfluidic organ-on-a-chip and gut-on-a-chip models continued in development to support reductionist studies of epithelial-bacterial and/or epithelial-immune cell interactions during mucosal barrier disruption. In fact, these models may allow personalized medicine studies in the future using patient-derived cells to evaluate injury and repair mechanisms. Work done in the past year evaluated the safety and efficacy of acid blocking drugs on ulcer healing, with new animal studies providing evidence that each drug affects the microbiome in a different way that can be correlated with its efficacy in ulcer healing. Lastly, work to understand the way in which mature epithelial cells or committed stem cells dedifferentiate, reprogram, proliferate, and then regenerate the gastroduodenal mucosa after injury was a major focus of studies in the past year. Summary Recent studies highlight novel mechanisms that promote restitution and mucosal regeneration after injury of the gastroduodenal mucosa.

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Total ginsenosides promotes intestinal epithelial proliferation via affecting polyamine-mediated HuR on post-transcriptional control

et al. 2023

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Polysaccharides from Panax ginseng promote intestinal epithelial cell migration through affecting the Ca2+ related regulators

Cited by 7 publications

References 20 publications

Exploring the Potential Mechanisms of Guanxinshutong Capsules in Treating Pathological Cardiac Hypertrophy based on Network Pharmacology, Computer-Aided Drug Design, and Animal Experiments

Exploring the Potential Mechanisms of Guanxinshutong Capsules in Treating Pathological Cardiac Hypertrophy based on Network Pharmacology, Computer-Aided Drug Design, and Animal Experiments

Pathophysiology updates: gastroduodenal injury and repair mechanisms

Total ginsenosides promotes intestinal epithelial proliferation via affecting polyamine-mediated HuR on post-transcriptional control

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