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P leurotus eryngii ( P . eryngii), also known as the king oyster mushroom, contains many bioactive substances, including polysaccharides, lipids, peptides, sterols and triterpenoids. The aim of this study was to explore the antitumor and immunomodulatory activities of P . eryngii extract. The fresh P . eryngii material was extracted with MeOH (methanol) and then partitioned with EtOAc (ethyl acetate). The study showed that the P . eryngii EtOAc extract ( EAe) not only has antitumor effects by in vitro and in vivo methods but also significantly increases some immune activities. In addition, histopathological observations showed that EAe-treated mice exhibited much lower cancerization throughout the liver and lung. EAe can also promote antioxidant activity, which may regulate the body's antioxidant capacity and activate the antitumor mechanism. Practical Applications Our study revealed the anticancer and immunomodulatory activity of P leurotus eryngii extract, and identified the key components of the P . eryngii extract with HPLC-MS. These findings explain the antitumor activity of P . eryngii, which is very useful for developing the potential antitumor drugs for clinical application. [ABSTRACT FROM AUTHOR]

Epidemiological studies have shown that exposure to ambient fine particulate matter (PM 2.5 ) is associated with an increased risk for cardiopulmonary diseases. The MEK5/ERK5 and NF-κB signaling pathways are closely related to the regulation of acute pulmonary cell injury (APCI) and may play an important role in the underlying pathophysiological mechanisms. Related studies have shown that Biochanin A (BCA) effectively interferes with APCI, but the underlying mechanism through which this occurs is not fully understood. Previously, based on proteomic and bioinformatic research, we found the indispensable role of MEK5 in mediating remission effects of BCA against PM 2.5 -induced lung toxicity. Therefore, using A549 adenocarcinoma human alveolar basal epithelial cells (A549 cells), we combined western blot and qRT-PCR to study the protective signaling pathways induced by BCA, indicating that MEK5/ERK5 and NF-κB are both involved in mediating APCI in response to PM 2.5 , and MEK5/ERK5 positively activated NF-κB and its downstream cellular regulatory factors. BCA significantly suppressed PM 2.5 -induced upregulation of MEK5/ERK5 expression and phosphorylation and activation of NF-κB. Furthermore, due to the specificity of the MEK5/ERK5 protein structure, the binding sites and binding patterns of BCA and MEK5 were analyzed using molecular docking correlation techniques, which showed that there are stable hydrogen bonds between BCA and the PB1 domain of MEK5 as well as its kinase domain. BCA forms a stable complex with MEK5, which has potential effects on MEKK2/3-MEK5-ERK5 ternary interactions, p62/αPKC-mediated NF-κB regulation, and inhibition of MEK5 target protein phosphorylation. Therefore, our study suggests that MEK5 is an important regulator of intracellular signaling of APCI in response to PM 2.5 exposure. BCA may exert anti-APCI activity by targeting MEK5 to inhibit activation of the MEK5/ERK5/NF-κB signaling pathway.

Haze pollution has become a global environmental problem, subsequently affecting air quality, climate, economy and human health. Notably, PM 2.5 (particulate matter with an aerodynamic diameter less than 2.5 micrometers) significantly accounts for a variety of adverse health effects, in particular pulmonary diseases such as asthma and lung cancer. Clinical diagnosis and medical treatment of the lung damage caused by PM 2.5 still remain significant challenges due to the lack of specific biomarkers and pathways. Here, we established a rat model of nonsurgical intratracheal instillation to investigate PM 2.5 exposure and employed iTRAQ based analytical technique and bioinformatics tools to identify putative biomarkers and pathways. We identified 163 differentially expressed proteins (DEPs). Among these proteins, we screened six DEPs (HMOX1, MP2K5, XRCC1 E9PTZ7, KNT2 and A1AG) as the putative biomarkers, with significant differentially expressed levels (percentage increment > 140%). Pathway analysis indicated that calcium signaling, MAPK and PI3K/AKT might be involved in the process of PM 2.5 -induced lung damage. Western-blotting was used to verify DEPs in the AEC-II cell model for early diagnosis. In summary, our data can serve as fundamental research clues for further studies of PM 2.5 -induced toxicity in the lungs., Competing Interests: The authors declare no competing financial interests., (This journal is © The Royal Society of Chemistry.)

The antitumor and antioxidative activities of a rapeseed protein hydrolysate (RSCH) obtained from rapeseed meal were evaluated by using an in vivo S180 tumor-bearing Kunming mice model. Tumor-bearing female mice were given RSCH for 10 at doses of 0, 50, 100, and 150 mg/kg/d by gastric perfusion. RSCH significantly decreased the tumor weight by 44% and 53% in the 100 and 150 mg/kg/d groups, respectively, without causing mortality or growth retardation. The thymus and spleen indices (organ weight relative to body weight) were increased significantly in the 150 mg/kg/d group. The phagocytic capability of coeliac macrophages and delayed-type hypersensitivity (DTH) were significantly increased in tumor-bearing mice treated with RSCH at 150 mg/kg/d. RSCH administration also enhanced the superoxide dismutase activity and reduced the serum level of thiobarbituric acid reactive substances. Our results show that an oral RSCH administration had an antitumor protective effect and may improve immune function by reducing free radical formation and oxidative stress in a murine model.