4‐Hydroxycinnamic acid suppresses airway inflammation and mucus hypersecretion in allergic asthma induced by ovalbumin challenge

Abstract

In this study, we investigated whether 4‐hydroxycinnamic acid (HA) has a palliative effect on asthmatic inflammatory responses using a mouse model of ovalbumin (OVA)‐induced allergic asthma. The mice were divided into five groups, each consisting of seven females (normal control phosphate‐buffered saline); OVA (OVA sensitization/challenge); dexamethasone (DEX, OVA sensitization/challenge + dexamethasone 3 mg/kg); HA‐10 and HA‐20 OVA sensitization/challenge + HA 10 and 20 mg/kg, respectively). Mice treated with HA showed a reduction in airway hyperresponsiveness and in the number of inflammatory cells in bronchoalveolar lavage fluid (BALF) compared with asthmatic control. HA treatment also reduced the levels of interleukin (IL)‐5 and IL‐13 in BALF and of OVA‐specific immunoglobulin E in the serum compared with asthmatic control. HA treatment relieved airway inflammation and mucus overproduction caused by OVA exposure. Additionally, HA inhibited the increases in levels of nuclear factor kappa B, inducible nitric oxide synthase, and cyclooxygenase‐2 that normally occur after OVA exposure. HA treatment also reduced the activity and protein level of matrix metalloproteinase‐9. Taken together, HA effectively suppressed asthmatic airway inflammation and mucus production caused by OVA exposure. These findings indicate that HA has the potential to be used as a therapeutic agent for asthma.

Integrative analysis of the gut microbiome and metabolome in a rat model with stress induced irritable bowel syndrome

“…The decreased abundance of these three metabolites in the stress-induced IBS rat model indicates that colonic immune instability might be affected. The increased metabolic of dl -3-Phenyllactic acid 60 and 4-Hydroxycinnamic acid 61 , 62 , which has many pharmacological properties including immune-modulatory, anti-inflammatory and antioxidant effects, may be involved in regulating the imbalance of intestinal immunity. These two isoforms of Phenylalanine, l .Phenylalanine and dl .Phenylalanine have similar physiological efficacy, and these were detected to be highly produced in the stress-induced model, indicating the low bioavailability of metabolites in the intestine of stress rats.…”

Inner Shell of the Chestnut (Castanea crenatta) Suppresses Inflammatory Responses in Ovalbumin-Induced Allergic Asthma Mouse Model

“…), and CIE L or H (OVA treatment + CIE 100 or 300 mg/kg, p.o., respectively). The allergic asthma mouse model was induced through OVA using the method described in our previous study [ 18 ]. Briefly, each mouse was immunized by 20 μg OVA (emulsified in 10 mg/mL of aluminum hydroxide and PBS) intraperitoneal injection on test days 0 and 14.…”

“…As described in the previous paper, MMP-9 activity was measured by the gelatin zymography test method [ 18 ]. In principle, blue-stained gel is visualized as a white band by dissolving gelatin where MMP-9 activity is high.…”

Implications for Extracellular Matrix Interactions With Human Lung Basal Stem Cells in Lung Development, Disease, and Airway Modeling

“…Studies have shown that HA is increased in both bronchioalveolar fluid ( Bousquet et al, 1991 ; Zhu et al, 2010 ; Ge et al, 2018 ) and in ECM produced when HBECs of asthmatics are cultured with human lung fibroblasts ( Reeves et al, 2018 ). Its ability to suppress airway inflammation and mucus secretion, indicating that HA may be a potential therapeutic option for reducing remodeling in asthma ( Ko et al, 2020 ).…”

“…Discrepancies may be attributed to the severity of the disease or localization of specific MMP responses ( Araujo et al, 2008 ), significant research still needs to be carried out in this area and likely requires the use of more complex, human tissue-level studies comprising of all the cells in an EMTU. MMP-9 and MMP-12 are increased in the airway smooth muscle of the large airways in fatal cases of asthma ( Araujo et al, 2008 ) and it has been shown that HA may play a role in suppressing MMP9 production and be of potential therapeutic benefit ( Ko et al, 2020 ). More recently a role for MMP2, expressed by HBECs, has been considered in ECM remodeling and data suggests that MMP2 may be key in mediating crosstalk between HBEC and their underlying myofibroblasts in the EMTU and that a net change in MMP2 activity in asthma may promote fibrosis and increased deposition of ECM, despite its role in ECM degradation ( Xu et al, 2002 ).…”