Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest

Wang, Dong; Zhang, Xinjie; Qu, Daoxu; Han, Jichun; Meng, Fanqing; Xu, Mingyuan; Zheng, Qi

doi:10.3892/mmr.2018.9254

Cited by 5 publications

(5 citation statements)

References 33 publications

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“…Therefore, DHM has been shown to have a variety of beneficial functions in the current study and has become a potential source of treatment of CIRI. A previous study investigating ischemia reperfusion injury found that DHM enhances protection during ischemia, decreases myocardial dysfunction by enhancing anti-inflammatory activities, attenuates myocardial oxidative injury and prevents apoptosis during ischemia/reperfusion (22). In a study investigating cerebral ischemia, DHM was found to effectively prevent cerebral edema caused by whole brain I/R injury in rats caused by the ligation of the bilateral common carotid artery (23).…”

Section: Discussionmentioning

confidence: 99%

Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

et al. 2021

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Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that ischemic injury of the brain leads to the injury of brain cells, which is further aggravated after the recovery of blood reperfusion. Dihydromyricetin (DHM) has an effective therapeutic effect on vascular diseases; however, its role in CIRI has not been investigated. The oxygen and glucose deprivation/reoxygenation (OGD/R) cell model was used on HT22 hippocampal neurons in mice, by oxygen and sugar deprivation. DHM was found to increase the cell viability of HT22 cells following OGD/R induction. The levels of malondialdehyde (MDA) decreased, superoxide dismutase (SOD) and glutathione (GSH) in the OGD/R-induced HT22 cells increased following DHM treatment, accompanied by the decreased protein expression levels of NOX2 and NOX4. DHM also inhibited cell apoptosis induced by OGD/R, and decreased the protein expression levels of Bax and caspase-3, and increased the expression levels of Bcl-2. Moreover, the expression levels of the NF-E2-related factor 2 (Nrf2)/heme oxygenase (HO-1) signaling pathway-associated proteins in OGD/R-induced HT22 were increased following DHM treatment, and the effect of DHM on oxidative stress and apoptosis was reversed after the addition of the Nrf2/HO-1 pathway inhibitor, brusatol. In conclusion, DHM inhibited oxidative stress and apoptosis in OGD/R-induced HT22 cells by activating the Nrf2/HO-1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

et al. 2021

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“…Astragalin isolated from mulberry leaves by glycosides could reduce hemolysis of red blood cells induced by oxygen free radicals (Choi et al, 2013). As auxiliary components, astragalin and dihydromyricetin can enhance the protective effects of histidine, tryptophan, and ketoglutarate during cardiac arrest (Wang et al, 2018). However, the anti-tumor activity of ASG and their main mechanism have rarely been reported.…”

Section: Discussionmentioning

confidence: 99%

Astragalin Inhibits the Proliferation and Migration of Human Colon Cancer HCT116 Cells by Regulating the NF-κB Signaling Pathway

Yang

Xie

et al. 2021

Front. Pharmacol.

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Astragalin is a flavonoid found in a variety of natural plants. It has anti-inflammatory, anti-oxidant effects and has inhibited effects against several malignant tumor cell types. However, its effects on colon cancer and the molecular mechanisms have remained to be elucidated. In this study, we evaluated the inhibitory effect of astragalin on proliferation and migration of human colon cancer HCT116 cells in vitro and in vivo. Furthermore, we elucidated the mechanism of these effects. The results showed that astragalin significantly inhibited the proliferation and diffusion of HCT116 cells by induced apoptosis (by modulation of Bax, Bcl-2, P53, caspase-3, caspase 6, caspase 7, caspase 8, caspase 9 protein express) and cell cycle arrest (by modulation of Cyclin D1, Cyclin E, P21, P27, CDK2, CDK4 protein express). Moreover, astragalin suppressed HCT116 cell migration by inhibiting the expression of matrix metalloproteinases (MMP-2, MMP-9). In addition, astragalin significantly downregulated the expression of key proteins in the NF-κB signaling pathway and inhibited the transcriptional activity of NF-κB P65 stimulated with inflammatory cytokines TNF-α, thereby inhibiting the growth of colon cancer cells in vitro. Our further investigations unveiled astragalin gavage significantly reduced the proliferation of colon cancer xenograft in nude mice, in vivo experiments showed that tumor growth was related to decreased expression of apoptotic proteins in tumor tissues and decreased activity of the NF-κB signaling pathway. In summary, our results indicated that astragalin inhibits the proliferation and growth of colon cancer cells in vivo and in vitro via the NF-κB pathway. Therefore, astragalin maybe become a potential plant-derived antitumor drug for colon cancer.

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“…The expression of IL-6 was also obviously reduced. Thereby, AST alleviated the inflammatory response caused by oxidative stress [64][65][66]. Furthermore, AST also showed promise in improving brain I/R injury.…”

Section: The Effect Of Astragalin On the Ischemia-reperfusion Injury ...mentioning

confidence: 96%

Research Progress on Anti-Inflammatory Effects and Related Mechanisms of Astragalin

Ruan,

Shi,

Cao

et al. 2024

IJMS

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Chronic inflammation is a significant contributor to the development of cancer, cardiovascular disease, diabetes, obesity, autoimmune disease, inflammatory bowel disease, and other illnesses. In the academic field, there is a constant demand for effective methods to alleviate inflammation. Astragalin (AST), a type of flavonoid glycoside that is the primary component in several widely used traditional Chinese anti-inflammatory medications in clinical practice, has garnered attention from numerous experts and scholars. This article focuses on the anti-inflammatory effects of AST and conducts research on relevant literature from 2003 to 2023. The findings indicate that AST demonstrates promising anti-inflammatory potential in various models of inflammatory diseases. Specifically, AST is believed to possess inhibitory effects on inflammation-related factors and protein levels in various in vitro cell models, such as macrophages, microglia, and epithelial cells. In vivo studies have shown that AST effectively alleviates neuroinflammation and brain damage while also exhibiting potential for treating moderate diseases such as depression and stroke; it also demonstrates significant anti-inflammatory effects on both large and small intestinal epithelial cells. Animal experiments have further demonstrated that AST exerts therapeutic effects on colitis mice. Molecular biology studies have revealed that AST regulates complex signaling networks, including NF-κB, MAPK, JAK/STAT pathways, etc. In conclusion, this review will provide insights and references for the development of AST as an anti-inflammatory agent as well as for related drug development.

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Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest

Cited by 5 publications

References 33 publications

Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

Astragalin Inhibits the Proliferation and Migration of Human Colon Cancer HCT116 Cells by Regulating the NF-κB Signaling Pathway

Research Progress on Anti-Inflammatory Effects and Related Mechanisms of Astragalin

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