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Objectives: In the study, we investigated the effects of an Eriocheir sinensis water extract on a reflux esophagitis-induced rat model. Background: The crab has been used as a traditional medicine and food source in many countries worldwide for a long time, and the crab contains various useful substances such as chitin, protein, calcium carbonate, etc. Materials and Methods: All rats were fasted for 24 h and then orally pretreated with saline, Eriocheir sinensis (100 mg/kg), or ranitidine (40 mg/kg). Reflux esophagitis was induced by pylorus and forestomach ligation. Morphological changes in the mucosal damage in the esophagus were analyzed by the ImageJ program. Also, the expression of the inflammatory proteins and cytokine in the esophagus was measured by western blot assay to demonstrate the protective effects of Eriocheir sinensis in reflux esophagitis model. Histological analysis of esophagus was performed by hematoxylin & eosin (H&E) staining. Results: In the reflux esophagitis induction group, the esophageal tissue damage caused by the induction of reflux was 60% of the whole. Eriocheir sinensis administration significantly ameliorated esophageal mucosal damage by 40%, also determined by histological evaluation of reflux esophagitis in rats. Eriocheir sinensis was also found to downregulate the expression levels of proteins such as cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and tight junction protein (claudin-5) compared to the reflux esophagitis induction group. In addition, Eriocheir sinensis markedly attenuated the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and the phosphorylation of the inhibitor of NF-κB (IκBα). Conclusion: These results indicated that Eriocheir sinensis suppressed the development of esophagitis and modulated inflammation by regulating NF-κB activation. Based on these findings, we concluded that Eriocheir sinensis can protect the esophageal mucosa from reflux esophagitis. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) is chronic allergic contact dermatitis with immune dysregulation. Veronica persica has pharmacological activity that prevents asthmatic inflammation by ameliorating inflammatory cell activation. However, the potential effects of the ethanol extract of V. persica (EEVP) on AD remain elusive. This study evaluated the activity and underlying molecular pathway of EEVP in two AD models: dinitrochlorobenzene (DNCB)-induced mice and interferon (IFN)-γ/tumor necrosis factor (TNF)-α-stimulated human HaCaT keratinocytes. EEVP attenuated the DNCB-induced increase in serum immunoglobulin E and histamine levels, mast cell counts in toluidine-blue-stained dorsal skin, inflammatory cytokine (IFN-γ, interleukin [IL]-4, IL-5, and IL-13) levels in cultured splenocytes, and the mRNA expression of IL6, IL13, IL31 receptor, CCR-3, and TNFα in dorsal tissue. Additionally, EEVP inhibited the IFN-γ/TNF-α-induced mRNA expression of IL6, IL13, and CXCL10 in HaCaT cells. Furthermore, EEVP restored the IFN-γ/TNF-α-induced downregulation of heme oxygenase (HO)-1 in HaCaT cells by inducing nuclear factor erythroid 2-related factor 2 (Nrf2) expression. A molecular docking analysis demonstrated that EEVP components have a strong affinity to the Kelch-like ECH-associated protein 1 Kelch domain. In summary, EEVP inhibits inflammatory AD by attenuating immune cell activation and inducing the Nrf2/HO-1 signaling pathway in skin keratinocytes. [ABSTRACT FROM AUTHOR]

Background: Reflux esophagitis (RE) is a type of gastroesophageal reflux disease (GERD) that severely reduces the quality of life. The Cudrania tricuspidata (C. tricuspidata) fruit is commonly used in food and has medicinal values such as clearing heat, relaxing muscles, and collaterals. Objectives: We evaluated fermented C. tricuspidata fruit extract (FCt) in this study. We measured its anti-inflammatory activity by using LPS-induced Raw 264.7 cell model and evaluated its role in improving acute reflux esophagitis in rats. Materials and Methods: The gastrodin content before and after fermentation was determined. NO production in cell supernatant was measured using the Griess reagent method, and TNF-α and IL-1β secretion was detected using the Quantikine ELISA kit. Expression level of proteins was measured by western blotting. Immunofluorescence assay was used for confirming the activation of NF-κB. The protective effects of FCt on RE were conducted in the rat RE model by observing esophageal tissue damage and inflammatory proteins expression levels in the esophagus. Results: The results showed that the content of gastrodin in C. tricuspidata fruit increased upon fermentation. FCt inhibited the production of NO, TNF-α, and IL-1β and the activation of NF-κB. In addition, FCt significantly improved esophageal tissue damage caused by acid reflux and inhibited the expression of inflammatory proteins iNOS and COX-2 in esophageal tissue. The term of tight junction (claudin-4) is increased to maintain the barrier function of cell tissues. Conclusion: We suggested that FCt could consider being a candidate medicine material for treating RE. [ABSTRACT FROM AUTHOR]

Gastroesophageal reflux disease (GERD) is a disease that stomach contents continually refluxing into esophagus causes symptoms and/or complications. The study was working to find natural plant extracts with good effects and small side effects to treat reflux esophagitis (RE). The anti-inflammatory effects of hexane extract of Magnolia sieboldii (MsHE) were conducted on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. The ameliorative effects of MsHE on esophageal damage in rats induced by gastric acid reflux was explored in vivo. The results showed that MsHE decreased the production of nitric oxide (NO) and expression levels of iNOS, COX-2 and TNF-α on LPS-stimulated RAW 264.7 cells and MsHE treatment ameliorated the rats' esophageal tissue damage induced by gastric acid and inhibited the increase of inflammatory mediators and pro-inflammatory cytokines by regulating NF-κB signaling pathway. In addition, MsHE protected the function of barrier of epithelial cells against inflammatory conditions through increasing the expression of tight junctions. Furthermore, liquid chromatography-mass spectrometry analysis was used for determine the active ingredients contained in MsHE. The results show that MsHE can alleviate experimental rat RE by regulating NF-κB signaling pathway. In summary, MsHE may be used as a source material of drug candidate for the treatment of RE. [ABSTRACT FROM AUTHOR]

Background: Reflux esophagitis (RE) is one of the gastroesophageal reflux diseases that seriously affect the daily life of patients. Magnolia sieboldii K. Koch has been used as a traditional Chinese herbal medicine for stomach pain relief and deworming and has various physiological activities. Objective: The objective is to investigate the anti-inflammatory and protective effects of the ethanol extract of M. sieboldii buds (MsE) on RE. Materials and Methods: The different concentrations of MsE were used to determine the anti-inflammatory effects on lipopolysaccharide (LPS)-induced cells. In addition, the treatment of MsE on experimental RE rats were used for determining the protective effects of MsE on RE. Results: M. sieboldii treatment effectively inhibited LPS-induced nitric oxide (NO) production, protein expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-α) by regulating the activation of nuclear factor-κB (NF-κB) and C-Jun N-terminal kinase/mitogen-activated protein kinase in cells. Furthermore, M. sieboldii treatment significantly ameliorated esophageal tissue damage caused by gastric acid reflux, as well as inhibited the expression of COX-2, TNF-α, and interleukin-1 beta in esophageal tissues through inhibition the activation of NF-κB. Conclusion: We suggested that the ethanol extract of M. sieboldii could consider being an alternative medicine material for treating RE. [ABSTRACT FROM AUTHOR]

Sigesbeckia pubescens (SP) is a traditional Chinese medicine, possessing antioxidant and anti-inflammatory activities. In this study, we evaluate the neuroprotective activities of SP extract on glutamate-induced oxidative stress in HT22 cells and the molecular mechanism underlying neuroprotection. We applied 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), crystal violet, reactive oxygen species (ROS), lactate dehydrogenase (LDH), quantitative real-time polymerase chain reaction (qPCR), and western blot analyses for assessing the neuroprotective effects of SP extract. The experimental study revealed that SP considerably increased the cell viability, and reduced the oxidative stress promoted ROS and LDH generation in HT22 cells in a dose-dependent manner. Additionally, the morphology of HT22 cells was effectively improved by SP. Upregulated gene expressions of mitogen-activated protein kinase (MAPK) were markedly attenuated by SP. Similarly, SP notably suppressed the ROS-mediated phosphorylation of MAPK (pERK1/2, pJNK, and pp38) cascades and activation of apoptotic factor caspase-3 signaling pathway that overall contributed to the neuroprotection. Taken together, SP may exert neuroprotective effects via alteration of MAPK and caspase-3 pathways under oxidative stress condition. Therefore, SP is a potential agent for preventing oxidative stress-mediated neuronal cell death. [ABSTRACT FROM AUTHOR]