Objective: To investigate the potential correlation of transforming growth factor-β (TGF-β), matrix metalloprotein 9 (MMP-9), tissue inhibitor of metalloproteinases 1 (TIMP-1), Interleukin 1 (IL-1), IL-4, IL-6, IL-17, and tumor necrosis factor alpha (TNF-α) in refractory chronic rhinosinusitis. Methods: A total of 150 participants were retrospectively included in this study from August 2018 to February 2020. The people enrolled were equally allocated into refractory group (patients with refractory chronic rhinosinusitis), chronic group (patients with chronic rhinosinusitis), and control group (normal people). The level of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α were recorded. The unconditional multivariate binary logistic regression was used to analyze the factors affecting refractory chronic rhinosinusitis. Results: The Davos score, T&T olfactometer threshold test, and Lund-Mackay CT scores in refractory group were significantly higher than the chronic group (P<0.05). The level of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α in the refractory group were significantly higher than the chronic group and the control group (all P<0.05). Similarly, the level of the above mentioned indexes in the chronic group were significantly higher than the control group (P<0.05). The Davos score, T&T olfactometer threshold test score, Lund-Mackay CT score, and the level of TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α positively correlated with refractory chronic rhinosinusitis. Moreover, the unconditional multivariate binary logistic regression showed that the influencing factors of refractory chronic rhinosinusitis included TGF-β1, MMP-9, TIMP-1, IL-1, IL-4, IL-6, IL-17, and TNF-α. Conclusion: The findings of the present study provide evidence for TGF-β1, MMP-9, TIMP-1, IL-4, IL-6, IL-17, and TNF-α as the influencing factors of refractory chronic rhinosinusitis.

Alzheimer's disease (AD) is a degenerative disease of the central nervous system. The pathogenesis of AD has been explained using cholinergic, β-amyloid toxicity, tau protein hyperphosphorylation, and oxidative stress theories. However, an effective treatment method has not been developed. In recent years, with the discovery of the brain-gut axis (BGA) and breakthroughs made in Parkinson's disease, depression, autism, and other diseases, BGA has become a hotspot in AD research. Several studies have shown that gut microbiota can affect the brain and behavior of patients with AD , especially their cognitive function. Animal models, fecal microbiota transplantation, and probiotic intervention also provide evidence regarding the correlation between gut microbiota and AD. This article discusses the relationship and related mechanisms between gut microbiota and AD based on BGA to provide possible strategies for preventing or alleviating AD symptoms by regulating gut microbiota.

Allergic rhinitis is one of the common chronic inflammatory diseases of the nasal mucosa. In order to investigate the effect of zinc on ovalbumin induced allergic rhinitis in BALB/C male mice based on NF-KB signaling pathway, thirty BALB/C male mice are randomly divided into three groups: control group, ovalbumin induced allergic rhinitis asthma group and zinc intervention group. The experimental results show that Zinc supplementation in allergic asthma mice with allergic rhinitis correct the immune response of TH2 cells by inhibiting THE NF-KB signaling pathway, reduce the infiltration of inflammatory cells into lung nasal tissue, and reduce airway co-hyperreactivity to improve the clinical symptoms of asthma and play an immune protective role.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory loss and cognitive dysfunction in the elderly, with amyloid-beta (Aβ) deposition and hyperphosphorylation of tau protein as the main pathological feature. Nuclear factor 2 (Nrf2) is a transcription factor that primarily exists in the cytosol of hippocampal neurons, and it is considered as an important regulator of autophagy, oxidative stress, and inflammation. Total saikosaponins (TS) is the main bioactive component of Radix bupleuri (Chaihu). In this study, it was found that TS could ameliorate cognitive dysfunction in APP/PS1 transgenic mice and reduce Aβ generation and senile plaque deposition via activating Nrf2 and downregulating the expression of β-secretase 1 (BACE1). In addition, TS can enhance autophagy by promoting the expression of Beclin-1 and LC3-II, increasing the degradation of p62 and NDP52 and the clearance of phosphorylated tau (p-tau), and reducing the expression of p-tau. It can also downregulate the expression of nuclear factor-κB (NF-κB) to inhibit the activation of glial cells and reduce the release of inflammatory factors. In vitro experiments using PC12 cells induced by Aβ, TS could significantly inhibit the aggregation of Aβ and reduce cytotoxicity. It was found that Nrf2 knock-out weakened the inhibitory effect of TS on BACE1 and NF-κB transcription in PC12 cells. Moreover, the inhibitory effect of TS on BACE1 transcription was achieved by promoting the binding of Nrf2 and the promoter of BACE1 ARE1. Results showed that TS downregulated the expression of BACE1 and NF-κB through Nrf2, thereby reducing the generation of Aβ and inhibiting neuroinflammation. Furthermore, TS can ameliorate synaptic loss and alleviate oxidative stress. In gut microbiota analysis, dysbiosis was demonstrated in APP/PS1 transgenic mice, indicating a potential link between gut microbiota and AD. Furthermore, TS treatment reverses the gut microbiota disorder in APP/PS1 mice, suggesting a therapeutic strategy by remodeling the gut microbe. Collectively, these data shows that TS may serve as a potential approach for AD treatment. Further investigation is needed to clarify the detailed mechanisms underlying TS regulating gut microbiota and oxidative stress.

Radix Bupleuri is a traditional medicine widely used in China and other Asian countries. Phytochemistry and pharmacology study reveal that saikosaponins(SSs) are the main bioactive compounds in Radix Bupleuri. SSs are complex compounds composed of triterpene aglycone and carbohydrate part containing 1-13 monosaccharides, which can be divided into seven types based on their structural characteristics. Many different kinds of SSs have been isolated from plants of Bupleurum L. SSs show a variety of biological activities, such as central nervous system protection, liver protection, antivirus, anti-tumor, anti-inflammation, hormone-like effects, and immune regulation functions. Due to their broad activity and favorable safety profile, SSs attract an increasing amount of attention in recent years. In this review, the structures of 86 SSs are summarized based on the different aglycones due to the diverse structures of saikosaponin(SS). The pharmacological effects and related mechanism of SSs are thoroughly reviewed, and perspectives for future research are further discussed.

Alzheimer's disease (AD) is the most common neurodegenerative disease associated with aging. Bupleurum smithii Wolff. is a Chinese folk medicine used to reduce fever and inflammation. Regarding the key role of neuroinflammation in AD pathogenesis, it was speculated that B. smithii may be the source of compounds that treat AD through anti-inflammatory effects. This study aimed to investigate the effects of saikogenin F, a natural active ingredient from B. smithii, on cognition impairment and neuroinflammation in AD mice induced by amyloid β (Aβ). The AD mice model was established by intracerebroventricular (i.c.v.) injection of Aβ, and different doses of saikogenin F (10, 20, and 40 mg/kg) were intragastrically administrated once daily. Results of behavioral experiments, including the novel object recognition (NOR) test, Y-maze test, and Morris water maze (MWZ) test, showed that saikogenin F could ameliorate Aβ-induced cognition impairment in AD mice. Enzyme linked immunosorbent assay (ELISA) results showed that tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and reactive oxygen species (ROS) levels in hippocampal tissue increased after Aβ injection, while saikogenin F could significantly reduce the concentrations of these inflammatory factors. Western blotting results revealed that the Aβ-induced reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits protein expression in mice hippocampus was remarkably downregulated by saikogenin F. Results of Iba-1 immunohistochemical staining showed that saikogenin F could effectively inhibit Aβ-induced activation of microglia in vivo. These results suggested that saikogenin F could relieve Aβ-induced cognitive impairment via inhibiting neuroinflammation and microglial activation. These effects may be achieved by inhibiting the expression of the NADPH oxidase subunits gp91phox and p47phox.