Berberine protects against esophageal mucosal damage in reflux esophagitis by suppressing proinflammatory cytokines

Choo, Byung-Kil; Roh, Seong‐Soo

doi:10.3892/etm.2013.1202

Cited by 20 publications

(15 citation statements)

References 37 publications

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“…Hence, the restoration of esophageal mucosa integrity represents an efficient and innocuous approach by which GERD could be alleviated. Accumulating studies exploring potential therapeutic targets have highlighted berberine and esophageal mucosal damage in reflux esophagitis caused by suppressing proinflammatory cytokines and cyclooxygenase-2, as well as reflux-related esophageal histological changes and the therapeutic use of melatonin in GERD [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Yu¹,

Wang²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Numerous studies have highlighted the activation of NF-κB in the esophageal mucosa during the early stages of gastroesophageal reflux disease (GERD). The present study aimed to investigate the role of the TLR4/NF-κB signaling pathway in GERD rat models. Methods: Wistar rats (n = 60) were recruited to establish a GERD animal model. Distal esophageal pH was assessed, followed by determination of the contents of thiobarbituric acid-reactive species (TBARS) and reactive oxygen species (ROS) in esophageal mucosa homogenate. ELISA was employed to detect the levels of inflammatory factors (IL-6, IL-8, IL-10 and TNF-α) in esophageal mucosa. The expression of MMP-3, MPP-9, Cldn1 and Cldn4 was determined by immunohistochemistry. RT-qPCR and western blot analysis were applied to evaluate the protein expressions in TLR4/NF-κB signaling pathway, while TUNEL staining was utilized to examine the apoptosis rate in the esophageal mucosal tissues. Results: Distal esophageal pH of the rats was higher in the GERD + PDTC group than in other groups. Levels of inflammatory factors in esophageal mucosal tissues were downregulated with the inhibition of NF-κB, which was determined to be associated with the decreased contents of TBARS and ROS. Moreover, decreased MMP-3 and MPP-9 in addition to elevated Cldn1 and Cldn4 were detected in the esophageal mucosa as a result of the inactivation of NF-κB. The TLR4/NF-κB signaling pathway-related proteins (TLR4, NF-κB and IκBα); the rate of apoptosis was demonstrated to be suppressed in the GERD + PDTC group, while inactivating NF-κB was found to alleviate the tissue damage observed in the esophageal mucosa. Conclusion: The key findings of the current study demonstrate that the inactivation of the TLR4/NF-κB signaling pathway alleviates oxidative stress injury and promotes the repair of esophageal mucosal injury among rats with GERD, highlighting a potential novel GERD mechanism.

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Section: Introductionmentioning

confidence: 99%

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Yu¹,

Wang²,

Zhang³

et al. 2018

Cell Physiol Biochem

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“…In clinical studies, OME can also act in reducing the effects of proinflammatory markers, such as IL-1β [56,72], monocyte chemoattractant protein-1 (MCP-1) [88], and IL-6 [87]. In cell cultures, esomeprazole has anti-inflammatory activity through mechanisms associated with suppression of proinflammatory proteins, including proteins of cell adhesion molecule 1, nitric oxide synthase, TNF-α, and interleukins (e.g., IL-1β and IL-6).…”

Section: Antioxidant and Anti-inflammatory Effects Several In Vivo Smentioning

confidence: 99%

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Paz

Alencar

Lima

et al. 2020

Oxidative Medicine and Cellular Longevity

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Omeprazole (OME) is commonly used to treat gastrointestinal disorders. However, long-term use of OME can increase the risk of gastric cancer. We aimed to characterize the pharmacological effects of OME and to correlate its adverse effects and toxicogenetic risks to the genomic instability mechanisms and cancer-based on database reports. Thus, a search (till Aug 2019) was made in the PubMed, Scopus, and ScienceDirect with relevant keywords. Based on the study objective, we included 80 clinical reports, forty-six in vitro, and 76 in vivo studies. While controversial, the findings suggest that long-term use of OME (5 to 40 mg/kg) can induce genomic instability. On the other hand, OME-mediated protective effects are well reported and related to proton pump blockade and anti-inflammatory activity through an increase in gastric flow, anti-inflammatory markers (COX-2 and interleukins) and antiapoptotic markers (caspases and BCL-2), glycoprotein expression, and neutrophil infiltration reduction. The reported adverse and toxic effects, especially in clinical studies, were atrophic gastritis, cobalamin deficiencies, homeostasis disorders, polyp development, hepatotoxicity, cytotoxicity, and genotoxicity. This study highlights that OME may induce genomic instability and increase the risk of certain types of cancer. Therefore, adequate precautions should be taken, especially in its long-term therapeutic strategies and self-medication practices.

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“…It has been shown that TNF-α and IL-1β by affecting, the epithelial and endothelial cells function contribute to the pathogenesis of inflammatory bowel disease (Crohn’s disease and ulcerative colitis) IBD as well as esophagitis (Andoh et al, 2008) (Choo and Roh, 2013). TNF-α and IL-1β induces inflammatory responses in vascular endothelium, which results in enhanced expression of cell adhesion molecules such as ICAM-1 and VCAM-1 (Andoh et al, 2008) (Choo and Roh, 2013) (Binion et al, 2009). These major cytokines also mediate the trans-migration of leukocytes to the endothelium leading to endothelial dysfunction and tissue damage.…”

Section: Discussionmentioning

confidence: 99%

Anti inflammatory and anti angiogenic effect of black raspberry extract on human esophageal and intestinal microvascular endothelial cells

Medda

Lyros

Schmidt

et al. 2015

Microvascular Research

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Polyphenolic compounds (anthocyanins, flavonoid glycosides) in berries prevent the initiation, promotion, and progression of carcinogenesis in rat’s digestive tract and esophagus, in part, via anti-inflammatory pathways. Angiogenesis has been implicated in the pathogenesis of chronic inflammation and tumorigenesis. In this study, we investigated the anti-inflammatory and anti-angiogenic effects of black raspberry extract (BRE) on two organ specific primary human intestinal microvascular endothelial cells, (HIMEC) and human esophageal microvascular endothelial cells (HEMEC), isolated from surgically resected human intestinal and donor discarded esophagus, respectively. HEMEC and HIMEC were stimulated with TNF-α/IL-1β with or without BRE. The anti-inflammatory effects of BRE were assessed based upon COX-2, ICAM-1 and VCAM-1 gene and protein expression, PGE2 production, NFκB p65 subunit nuclear translocation as well as endothelial-leukocyte adhesion. The anti-angiogenic effects of BRE were assessed on cell migration, proliferation and tube formation following VEGF stimulation as well as on activation of Akt, MAPK and JNK signaling pathways. BRE inhibited TNF-α/IL-1β-induced NFκB p65 nuclear translocation, PGE2 production, up-regulation of COX-2, ICAM-1 and VCAM-1 gene and protein expression and leukocyte binding in HEMEC but not in HIMEC. BRE attenuated VEGF-induced cell migration, proliferation and tube formation in both HEMEC and HIMEC. The anti-angiogenic effect of BRE is mediated by inhibition of Akt, MAPK and JNK phosphorylations. BRE exerted differential anti-inflammatory effects between HEMEC and HIMEC following TNF-α/IL-1β activation whereas demonstrated similar anti-angiogenic effects following VEGF stimulation in both cell lines. These findings may provide more insight into the anti-tumorigenic capacities of BRE in human disease and cancer.

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Berberine protects against esophageal mucosal damage in reflux esophagitis by suppressing proinflammatory cytokines

Cited by 20 publications

References 37 publications

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Anti inflammatory and anti angiogenic effect of black raspberry extract on human esophageal and intestinal microvascular endothelial cells

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