Cordyceps militaris solid medium polysaccharides (CMMPs) were extracted using an ultrasound-assisted enzyme method, and the process conditions were optimized via response surface methodology (RSM). The CMMPs were separated into four components named CMMP−1, CMMP−2, CMMP−3 and CMMP−4 using ethanol fractional precipitation, and their monosaccharide composition and structural properties were analyzed by molecular weight analysis, Fourier-transform infrared spectroscopy (FT–IR), scanning electron microscopy (SEM), Congo red test, ultraviolet–visible spectroscopy (UV-vis), atomic force microscopy (AFM), and thermogravimetric analysis (TGA). RSM could predict the yield of the CMMP (R² = 0.9928), and the polysaccharide yield was 15.43% under the selected conditions of 3.1% cellulase enzyme addition, a liquid–solid ratio of 42:1, an extraction temperature of 61 °C, and an extraction time of 60 min. Glucose and galactose were the main constituents of the four fractional precipitated polysaccharides. Furthermore, four components exhibited antioxidant activity, and CMMP−1 demonstrated stronger antioxidant activity in vitro. This study demonstrates the possibility of developing a natural antioxidant food from Cordyceps militaris solid medium.

Salmonella typhimurium (S.T) induces damage to the central nervous system; however, the role of Asiatic acid (AA) in this is still unknown. Microglia play a role as macrophages to recognize the invaded pathogenic microbes in the brain. The aim of this study was to investigate the protective effect and mechanism of AA on the central nervous system through an in vitro model of S.T infection in microglia. We pre-treated microglia with AA before S.T infection and explored the anti-infection mechanism of AA by sequencing, quantitative reverse transcription PCR (RT-qPCR), and Western blotting. Long non-coding RNA (lncRNA) sequencing demonstrated that inflammation is a major factor in S.T infection of microglia. RT-qPCR data demonstrated that AA inhibited S.T-induced increases in the mRNA levels of the pro-inflammatory factors interleukin (IL)-1β, IL-6, and IL-18. Western blotting demonstrated that AA inhibited S.T-induced activation of the nuclear factor (NF)-κB pathway and activation of the NLR family, pyrin domain-containing 3 (NLRP3) inflammasome. Expression of the lncRNA TVX1 in microglia was decreased by S.T infection and increased by pretreatment with AA. Inhibition of TVX1 expression reversed the anti-inflammatory effect of AA, and overexpression of TVX1 in microglia suppressed S.T-induced inflammation. In conclusion, AA attenuated S.T-induced microglial inflammation by upregulating the expression of the lncRNA TVX1.

Acute lung injury (ALI) is a common respiratory disease, Cordycepin has been reported to reduce ALI, which is an effective component in Cordyceps militaris solid medium extract (CMME). Therefore, we aimed to explore the alleviating effect and mechanism of CMME on ALI. This study evaluated the effect of CMME on lipopolysaccharide (LPS)-induced ALI mice by analyzing intestinal flora and metabolomics to explore its potential mechanism. We assessed pulmonary changes, inflammation, oxidative stress, and macrophage and neutrophil activation levels, then we analyzed the gut microbiota through 16S rRNA and analyzed metabolomics profile by UPLC-QTOF/MS. The results showed that CMME treatment improved pulmonary injury, reduced inflammatory factors and oxidative stress levels, and decreased macrophage activation and neutrophil recruitment. The 16S rRNA results revealed that CMME significantly increased gut microbiota richness and diversity and reduced the abundance of Bacteroides compared with Mod group significantly. Metabolic analysis indicated that CMME reversed the levels of differential metabolites and may ameliorate lung injury through purine metabolism, nucleotide metabolism, and bile acid (BA) metabolism, and CMME did reverse the changes of BA metabolites in ALI mice, and BA metabolites were associated with inflammatory factors and intestinal flora. Therefore, CMME may improve lung injury by regulating intestinal flora and correcting metabolic disorders, providing new insights into its mechanism of action.

Bovine viral diarrhea (BVD) is a common viral disease in cattle that causes huge economic losses in naïve herds that are introduced to bovine viral diarrhea virus (BVDV). Currently, there are no available anti-BVDV drugs due to the variety and mutability of strains; therefore, developing new anti-BVDV drugs is of great significance. The aim of this study was to investigate the anti-BVDV effects and immunomodulatory activities of Codonopsis pilosula polysaccharides (CPPs) in BVDV-infected bovine macrophage (BoMac) cells. CPPs directly inactivated BVDV particles and intervened in BVDV absorption process. The immunity suppression resulting from BVDV in BoMac cells was restored by CPPs, as was verified by phagocytosis increase, the expression up-regulation of cell surface co-stimulatory molecules (CD40, CD80, and CD86), and antigen-presenting function recovery. Furthermore, the expressions of cytokines including TNF-α, IFN-γ, IL-6, IL-18, IL-1β, Caspase-3, Bim, and Bcl-xL at the mRNA and proteins levels were modulated, and a reduction in the apoptosis rate was observed, which demonstrates that CPPs attenuated inflammation and apoptosis induced by BVDV. Collectively, our findings reveal new pharmacological properties of CPPs, which exert anti-BVDV efficacy and regulate immune injury induced by BVDV in BoMac cells, indicating that CPPs are a potential option for BVDV prevention in clinical application.

Curcumin, the principal bioactive compound derived from turmeric, possesses a wide range of therapeutic properties such as anti-inflammatory, antioxidant, and wound-healing properties. Recent studies suggest that curcumin may alleviate HMGB1-mediated inflammation in ovarian cells. However, its role in modulating dysfunction in HMGB1-driven ovarian granulosa cells (OGCs) remains to be elucidated. In the present study, curcumin suppresses the HMGB1-induced overexpression of toll-like receptor 2 (TLR2) and ovulation-related factors such as EGFR, VEGF, STAR, and TIMP1/2 genes. Additionally, the elevated levels of TLR2, TLR1, TLR6, and phospho-NF-κB p65 proteins were significantly inhibited by curcumin. Further mechanistic analysis reveals that the interaction between HMGB1 and the TLR1-TLR2/TLR6 complex, as well as phospho-NF-κB p65, was restrained. This resulted in the suppression of the pro-inflammatory cytokine IL-6 production and the alleviation of the HMGB1-induced inflammation response in OGCs. Collectively, our findings demonstrate that curcumin modulates the upregulation of ovulation-related genes and pro-inflammatory cytokines in OGCs by inhibiting the TLR2-NF-κB pathway, providing a mechanistic basis for its potential application as a therapeutic agent against OGC inflammation.