Diabetes mellitus has become a major global health problem due to increasing morbidity among all age groups. It has been reported that the number of patients with diabetes was more than 450 million in 2017, and would reach to 693 million on 2045 (Makinde et al., 2019). Diabetes mellitus is considered as a chronic and systemic metabolic disease which is associated with insulin deficiency (type 1) and insulin resistance or insulin insensitiveness (type 2) (Chausmer, 1998; De Liefde et al., 2005). The high blood glucose level could lead to hypertension, hyperlipidemia, weight gain, or obesity (Ahmed et al., 2019). It is well known that the destruction of pancreatic β cells can cause insulin deficiency and further develop into diabetes (Yoon & Jun, 2005). The pancreatic β cells are highly sensitive toward oxidative stress, which
The activation and degranulation of immune cells play a pivotal role in allergic inflammation, a pathological condition that includes anaphylaxis, pruritus, and allergic march-related diseases. In this study, trifuhalol A, a phlorotannin isolated from Agarum cribrosum, inhibited the degranulation of immune cells and the biosynthesis of IL-33 and IgE in differentiated B cells and keratinocytes, respectively. Additionally, trifuhalol A suppressed the IL-33 and IgE-mediated activation of RBL-2H3 cells through the regulation of the TAK1 and MK2 pathways. Hence, the effect of trifuhalol A on allergic inflammation was evaluated using a Compound 48/80-induced systemic anaphylaxis mouse model and a house dust mite (HDM)-induced atopic dermatitis (AD) mouse model. Trifuhalol A alleviated anaphylactic death and pruritus, which appeared as an early-phase reaction to allergic inflammation in the Compound 48/80-induced systemic anaphylaxis model. In addition, trifuhalol A improved symptoms such as itching, edema, erythema, and hyperkeratinization in HDM-induced AD mice as a late-phase reaction. Moreover, the expression of IL-33 and thymic stromal lymphopoietin, inflammatory cytokines secreted from activated keratinocytes, was significantly reduced by trifuhalol A administration, resulting in the reduced infiltration of immune cells into the skin and a reduction in the blood levels of IgE and IL-4. In summarizing the above results, these results confirm that trifuhalol A is a potential therapeutic candidate for the regulation of allergic inflammation.
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