Objective: Allergic rhinitis (AR) is primarily regulated by type I hypersensitivity, with Th2 and immunoglobulin E (IgE) playing essential roles. This study aimed to determine whether angiotensin converting enzyme (ACE)2 could participate in the regulation of AR. Methods: Nasal mucosal tissues of AR patients were collected to determine ACE2 levels. Following AR mouse models were established, ACE2 levels in nasal mucosa were determined. Then the influences of diminazene aceturate (ACE2 agonist) on AR symptoms, pathology, specific antibodies, histamine, and interleukins (ILs) release in vivo were evaluated. Afterward, human nasal mucosa epithelial cells were exposed to IL-13, and the impacts of ACE2 overexpression on the secretion of pro-inflammatory factors in vitro were assessed. Results: ACE2 levels significantly declined in nasal mucosa both in patients and mouse models (p < .001). Diminazene aceturate treatment elevated the ACE2 level in mice (p < .01), accompanied by reduced frequency of nasal spray and nasal friction, decreased eosinophils and goblet cells (p < .001) according to histopathological staining. Furthermore, lgE, lgG1, histamine, and IL levels in mice were also decreased (p < .05). In vitro experiments revealed that ACE2 overexpression suppressed the secretion of proinflammatory factors (p < .001). Conclusion:Together, ACE2 activation can alleviate the symptoms of AR in mice and inhibit the release of Th2 cytokines. Activating ACE2 is a promising therapeutic approach for AR.

Targeted therapy is an important therapeutic strategy currently, however, the development of targeted therapy for nasopharyngeal carcinoma (NPC) is relatively lagging. Cullin 4A (CUL4A) was reported to be overexpressed in NPC; nevertheless, the specific role of CUL4A remains unrevealed. NPC cells and tumor-bearing mice were cultivated to explore the role and mechanism of CUL4A in NPC. After evaluating CUL4A levels in NPC cells, functional experiments were carried out to investigate the effects of CUL4A knockdown and overexpression on cell proliferative, invasive and migratory aptitude as well as NF-κB signaling. Following the GeneMANIA database predicted that protein arginine methyltransferase 5 (PRMT5) was downstream of CUL4A, the mediated role of PRMT5 in the regulation of CUL4A on cells was then determined. Moreover, the tumor volumes and weights of tumor-bearing mice were recorded, and the levels of proliferation-, migration-, and NF-κB signaling-related proteins in the tumor were determined. Herein, CUL4A was enhanced in NPC cells, and its knockdown and overexpression separately suppressed and promoted cell proliferative, invasive, and migratory aptitude as well as NF-κB signal activation. Novelty, PRMT5 knockdown reversed the influences of CUL4A overexpression on these aspects. In addition, its knockdown likewise reversed the facilitating impact of CUL4A expression on tumor growth and declined the expression levels of proliferation-, migration-, and NF-κB signaling-related protein in the tumor. Together, this paper indicated that CUL4A promoted the proliferative, invasive, and migratory aptitude of NPC cells as well as tumor growth by promoting PRMT5 to activate NF-κB signaling.