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Shufeng Jiedu capsule (SFJDC) has been widely used as a conventional Chinese pharmaceutical agent for various upper respiratory infections, including acute lung injury, acute respiratory distress syndrome and allergic rhinitis (AR). However, its mechanism in AR remains unclear.The present study aimed to decipher the antiallergic inflammatory effect of SFJDC in an AR model with olfactory dysfunction. Specifically, we wanted to explore whether SFJDC can improve the olfactory abnormality in AR mice and reduce the levels of inflammatory factors in the olfactory epithelium (OE) and olfactory bulb (OB).To address the above issues, we constructed an AR model using C57BL/6 mice, which were sensitised and challenged with ovalbumin (OVA) by intraperitoneal injection. SFJDC (0.045 or 0.18 g/kg) was delivered by gavage administration 1 h prior to the intraperitoneal injection of OVA. The control mice received saline alone. Then, the animals were assessed according to the presence of nasal symptoms and nasal inflammation, and a buried food test was used to evaluate olfactory function. The levels of proteins involved in the AMPK/mTOR autophagy pathway in the OE and OB were investigated by western blotting and fluorescence staining.After OVA induction of AR and drug administration, we found that SFJDC significantly ameliorated the nasal symptoms and allergic inflammatory reaction of the nasal mucosa superior to cetirizine. A behavioural test indicated that the mice with AR had olfactory dysfunction, and SFJDC can ameliorate this behavior deficiency. Meanwhile, SFJDC clearly reduced the neuroinflammation level in OE tissue. In addition, SFJDC increased p-mTOR and decreased p-AMPK, beclin1, LC3 and cleaved caspase-3 levels in the OE.In addition to antibacterial and antiviral activities, SFJDC has marked anti-inflammatory effects in AR mice. Its mechanism of action in the nasal cavity involves inhibition of upregulated anti-inflammatory cytokines, modulation of autophagy and apoptosis levels and regulation of autophagy through the AMPK/mTOR pathway in the OE tissue of AR mice. Hence, SFJDC is a promising drug for AR, and clinical trials should further validate the therapeutic impact of SFJDC on AR with olfactory dysfunction.

Alzheimer's disease (AD) is a neurodegenerative disorder, which has become the leading cause of dementia cases globally. Synaptic failure is an early pathological feature of AD. However, the cause of synaptic failure in AD, especially the GABAergic synaptic activity remains unclear. Extensive evidence indicates that the presence of soluble amyloid-β is an early pathological feature in AD, which triggers synaptic dysfunction and cognitive decline. Our recent study explored the relation of GABAergic transmission and soluble Aβ in early APP/PS1 mice. Firstly, we found soluble Aβ42 levels were significantly increased in serum, hippocampus and prefrontal cortex in 3-4 months APP/PS1 mice, which was much earlier than Aβ plagues formation. In addition, we found TNF-α and BDNF expression levels were increased, while KCC2 and GABAAR expression were decreased in 3-4 months APP/PS1 hippocampus. When we treated 3-4 months APP/PS1 mice with a potent γ-secretase inhibitor, LY411575, which can reduce the soluble Aβ42 levels, the TNF-α and BDNF protein levels were decreased, while KCC2 and GABAAR levels were increased. In conclusion, our study suggested soluble Aβ may impaired the GABA inhibition by mediating KCC2 levels in early APP/PS1 mice. KCC2 may be served as a potential biomarker for AD.

Induced goblet cells are useful for studying the interaction of intestinal mucus layer and the gut microbiota., Intestinal goblet cells secrete mucus layers protecting the intestinal epithelia against injuries. It is challenging to study the interaction of goblet cells, mucus layers, and gut microbiota because of difficulty in producing goblet cells and mucus models. We generate intestinal goblet cells from human epidermal stem cells with two small molecular inhibitors Repsox and CHIR99021 in the presence of basic fibroblast growth factor and bone morphogenetic protein 4 at high efficiency (~95%) of conversion for a short time (6 to 8 days). Induced goblet cells are functional to secrete mucus, deliver fluorescent antigen, and form mucus layers modeling the mucus-microbe interaction in vitro. Transplantation of induced goblet cells and oral administration of chemical induction media promote the repair of the intestinal epithelia in a colitis mouse model. Thus, induced goblet cells can be used for investigating mucus-microbe interaction, and chemical cocktails may act as drugs for repairing the intestinal epithelia.

Shufengjiedu capsules (SFJDCs), a traditional Chinese medicine, have been widely used as an antiviral, antibacterial, antitumor, and anti-inflammatory drug. However, the roles of SFJDCs in allergic rhinitis remain unclear. The purpose of this study was to investigate the effects of SFJDCs in olfaction and lung injury in rats with allergic rhinitis. An animal model of allergic rhinitis was created by intraperitoneal injection and intranasal administration of ovalbumin to rats. All rats were divided into seven groups: a model group, a low-dose SFJDC group, a medium-dose SFJDC group, a high-dose SFJDC group, a cetirizine group, and a control group. Hematoxylin and eosin (HE) staining was used to observe pathological changes in rat lung and olfactory epithelium (OE) tissue, and peripheral blood was collected and subjected to an enzyme-linked immunosorbent assay (ELISA) to detect IgE, tumor necrosis factor alpha (TNF-α), and IL-1ꞵ levels. Western blotting, immunohistochemistry staining, and immunofluorescence staining were performed to detect inflammatory cytokines and levels of the autophagy biomarker beclin1 and the apoptosis biomarker cleaeved-caspased3 in lung and OE tissue. ELISA indicated that SFJDCs significantly decreased IgE, TNF-α, and IL-1ꞵ levels in peripheral blood, the lungs, and OE tissue. In addition, Western blotting and staining indicated that SFJDCs repair lung injury, protect against neuronal apoptosis in OE, and rescue impaired autophagy in the lungs and OE tissue. In conclusion, results indicated that SFJDCs might protect against neuronal loss in the OE and lung injury by enhancing autophagy and decreasing apoptosis in rats with allergic rhinitis. Therefore, SFJDCs might serve as an alternative treatment for allergic rhinitis.