2019
DOI: 10.1016/j.ejphar.2019.172720
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Isorhamnetin alleviates esophageal mucosal injury in a chronic model of reflux esophagitis

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Cited by 14 publications
(10 citation statements)
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“…Moreover, isorhamnetin decreased TNF‐α‐induced ERK, JNK, and p38 phosphorylation in a dose‐dependent manner and did not affect TNF‐α receptor expression on the surface in BEAS‐2B cells, suggesting that it inhibits airway epithelial inflammation and proliferation and migration by suppressing the MAPK pathway. Consistent with our data, studies in pancreatic cancer cells have shown that isorhamnetin inhibits cancer cell proliferation by blocking the MAPK signaling pathway (Wang et al, 2018), and it has been shown to reduce esophageal mucosal inflammatory injury in rats with reflux esophagitis by inhibiting the MAPK pathway (Liu et al, 2019).…”
Section: Discussionsupporting
confidence: 91%
“…Moreover, isorhamnetin decreased TNF‐α‐induced ERK, JNK, and p38 phosphorylation in a dose‐dependent manner and did not affect TNF‐α receptor expression on the surface in BEAS‐2B cells, suggesting that it inhibits airway epithelial inflammation and proliferation and migration by suppressing the MAPK pathway. Consistent with our data, studies in pancreatic cancer cells have shown that isorhamnetin inhibits cancer cell proliferation by blocking the MAPK signaling pathway (Wang et al, 2018), and it has been shown to reduce esophageal mucosal inflammatory injury in rats with reflux esophagitis by inhibiting the MAPK pathway (Liu et al, 2019).…”
Section: Discussionsupporting
confidence: 91%
“…This evidently indicates anti-inflammatory potential of isorhamnetin after a challenge of APAP. Consistent with this outcome, it has been demonstrated that isorhamnetin can promote functional recovery in a rat model of spinal cord injury by attenuation of oxidative stress and inflammatory responses [42] and can properly lower inflammatory factors such as IL-6, TNFα, and IL-1β in a model of reflux esophagitis [43].…”
Section: Discussionmentioning
confidence: 69%
“…Our study found that they were both the key targets of AM in the treatment of GU and had good binding affinity with all key ingredients. Meanwhile, evidence from existing studies has also confirmed that the screened key ingredients attenuated gastric mucosal inflammation by downregulating the expression of these two proinflammatory factors [ 48 50 ]. Furthermore, MAPK signaling pathway and PI3K-AKT signaling pathway have been already verified to ameliorate GU by regulating proinflammatory cytokines, and our study revealed that the common targets between AM and GU are enriched in these two pathways [ 51 , 52 ].…”
Section: Discussionmentioning
confidence: 99%