How do the main components influence the VOCs emission characteristics and formation pathways during moso bamboo heat treatment?

Bamboo heat treatment will cause plenty of release of volatile organic compounds (VOCs) into the atmosphere which are important precursors for ozone (O3) formation. In this study, dewaxed bamboo was heat-treated at 180 °C for 2 h to investigate the emission characteristics and the formation pathways of VOCs during heat treatment by removing different main components. The results showed that aldehydes (22.61%-57.54%) and esters (14.64%-38.88%) are the primary VOCs released during heat treatment. These compounds mainly originate from the degradation of hemicellulose, lignin, cellulose, and the linkage bonds between them in bamboo. During the bamboo heat treatment, the degradation of CO, CH, and CO bonds in hemicellulose results in the release of 5-hydroxymethylfurfural, 3-furfural, and 1-(+)-ascorbic acid 2,6-dihexadecanoate. The breakage of benzene ring group and the CO and CH bonds of lignin leading to the emission of VOCs including m-Formylphenol, Vanillin, and Syringaldehyde. The degradation of aliphatic CH, CC, and CO bonds in the amorphous region of cellulose contributes to an enhanced release of alcohols, olefins, and alkanes. It is calculated that acids (28.92%-59.47%), esters (10.10%-22.03%) and aldehydes (17.88%-39.91%) released during heat treatment contributed more to Ozone Formation Potential (OFP).

[Analysis on "the essence of tuina, arrival of qi ensuring curative effect"].

In reference with the systematic review of the thought of deqi (arrival of qi) put forward in Huangdi Neijing (Internal Classic of Yellow Emperor) and other classic books of traditional Chinese medicine, in view of detecting qi and identifying qi before treatment, as well as the prerequisites of deqi in tuina, meaning the accurate syndrome differentiation and manipulations, the importance of deqi in treatment with tuina is expounded. In association with clinical experience, the specific manifestations of deqi in patients during tuina are summarized, e.g. soreness, distention, pain, numbness, warm feeling and slight sweating, local changes in intestinal sound and skin color, as well as mind regulation. It is anticipated that deqi of tuina may be drawn the attention in clinical practice, and the relevant study be expanded.

Proapoptotic Effect of Icariin on Human Ovarian Cancer Cells via the NF-[Formula: see text]B/PI3K-AKT Signaling Pathway: A Network Pharmacology-Directed Experimental Investigation.

Based on network pharmacology tools and public bioinformatics databases, the pharmacodynamic target and key mechanism of icariin (ICA) in the treatment of ovarian cancer (OC) were identified and experimentally verified. Our previous research showed that TNF, MMP9, STAT3, PIK3CA, ERBB2, MTOR, IL2, PTGS2, KDR and F2 are important targets of ICA in the treatment of OC. TNF, as a hub gene in tumor tissues, was associated with poor prognosis. ICA acted on OC mainly through the biological functions of various kinases, and the pathway with the highest accuracy ([Formula: see text]-value) was PI3K. Meanwhile, we observed a close upstream and downstream relationship between NF-[Formula: see text]B and the Pl3K-AKT pathway. This study further verified the mechanism of ICA in promoting apoptosis of SKOV3 cells through the NF-[Formula: see text]B signaling pathway and the tandem relationship between NF-[Formula: see text]B and the Pl3K-AKT pathway. The assay results demonstrated that ICA can promote the apoptosis of SKOV3 cells as indicated by the proapoptotic markers Bax, Bcl-xl and Caspase-3 and the key factors of the NF-[Formula: see text]B signaling pathway (NF-[Formula: see text]Bp65, p-NF-[Formula: see text]Bp65, p-I[Formula: see text]B[Formula: see text] and I[Formula: see text]B[Formula: see text]. ICA can block the classical NF-[Formula: see text]B pathway by inhibiting I[Formula: see text]B[Formula: see text] phosphorylation and consequently blocking the activation of the NF-[Formula: see text]B pathway in SKOV3 cells. ICA can also promote apoptosis by blocking the activation of the NF-[Formula: see text]B pathway in SKOV3 cells via inhibition of NF-[Formula: see text]Bp65 nuclear translocation. After using a PI3K pathway inhibitor, we further discovered that ICA may reduce AKT signal transduction by inhibiting the level of Akt phosphorylation, resulting in a loss of PI3K/Akt-dependent activation of the NF-[Formula: see text]B pathway.

Study on the regulatory mechanism and experimental verification of icariin for the treatment of ovarian cancer based on network pharmacology.

ETHNOPHARMACOLOGICAL RELEVANCE: Herba Epimedii (Berberidaceae) has the advantages of "nourishing the kidney and reinforcing the Yang". Many species in this genus have long been used in traditional Chinese medicine (TCM) and have been used as anticancer drugs in traditional Chinese herbal medicine formulations. Icariin, a major flavonoid glycoside extracted from Epimedium brevicornum Maxim, has been widely proven to exert an inhibitory effect on ovarian cancer (OC), and icariin can induce apoptosis and inhibit invasion and migration. However, the underlying mechanism remains unclear, so further research is necessary to verify its traditional use. AIM OF THE STUDY: This study aimed to explore the regulatory mechanism of icariin in the biological network and signalling pathway of OC through network pharmacology and cytological experiments. METHODS: Public databases and R × 3.6.2 software were adopted to predict the potential targets, construct the protein-protein interaction (PPI) network, and perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. After the network pharmacological analysis, cytological experiments, real-time quantitative PCR (qPCR) and Western blot (WB) analyses were used to verify the key signalling pathway. RESULTS: The targets related to treatment were TNF, MMP9, STAT3, PIK3CA, ERBB2, MTOR, IL2, PTGS2, KDR, and F2. GO and KEGG enrichment analyses indicated that various kinases and the PI3K/AKT signalling pathway were the most enriched molecules and pathways. Icariin inhibited OC SKOV3 cell proliferation, migration and invasion in vitro and promoted apoptosis by inhibiting the PI3K/AKT signalling pathway. CONCLUSION: Icariin promotes apoptosis and suppresses SKOV3 cell activities through the PI3K-Akt signalling pathway. This research not only provides a theoretical and experimental basis for more in-depth studies but also offers an efficient method for the rational utilization of a series of icariin flavonoids as anti-tumour drugs.

Antifibrotic Mechanism of Cinobufagin in Bleomycin-Induced Pulmonary Fibrosis in Mice.

Idiopathic pulmonary fibrosis (IPF) is a progressive and usually fatal lung disease that is characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture and the formation of focal fibrous hyperplasia. The molecular mechanism by which pulmonary fibrosis develops is not fully understood, and no satisfactory treatment currently exists. However, many studies consider that aberrant activation of TGF-ß1 frequently promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. Cinobufagin (CBG), a traditional Chinese medicine, has been widely used for long-term pain relief, cardiac stimulation, and anti-inflammatory and local anesthetic treatments. However, its role in pulmonary fibrosis has not yet been established. We investigated the hypothesis that cinobufagin plays an inhibitory role on TGF-ß1 signaling using a luciferase-reporter assay. We further explored the effect of cinobufagin on pulmonary fibrosis both in vitro and in vivo. The in vitro experiments showed that cinobufagin suppresses TGF-ß1/Smad3 signaling in a dose-dependent manner, attenuates the activation and differentiation of lung fibroblasts and inhibits EMT induced by TGF-ß1 in alveolar epithelial cells. The in vivo experiments indicated that cinobufagin significantly alleviates bleomycin-induced collagen deposition and improves pulmonary function. Further study showed that cinobufagin could attenuate bleomycin-induced inflammation and inhibit fibroblast activation and the EMT process in vivo. In summary, cinobufagin attenuates bleomycin-induced pulmonary fibrosis in mice via suppressing inflammation, fibroblast activation and epithelial-mesenchymal transition.

[Study on liver protection and hepatotoxicity of saikosaponin a based on zebrafish model].

Bupleuri Radix has both liver protection and hepatotoxicity. Saponins are the main pharmacodynamic and toxic components of Bupleuri Radix. Based on zebrafish physical model and the model of alcoholic fatty liver( AFL) pathology,the liver toxic and protective effect of saikosaponin a( SSa) were assessed. The results indicated that 1. 77 µmol·L-1 SSa showed protective effect to AFL zebrafish. 5. 30 µmol·L-1 SSa was hepatotoxic to healthy zebrafish,but it showed protective effect to AFL zebrafish. 5. 62 µmol·L-1 SSa was hepatotoxic to healthy and AFL zebrafish. This study is benefit for clinical safety of saikosaponin a.

Parthenolide attenuated bleomycin-induced pulmonary fibrosis via the NF-κB/Snail signaling pathway.

BACKGROUND: Parthenolide (PTL) is a natural molecule isolated from Tanacetum parthenium that exhibits excellent anti-inflammatory and antitumor activities. Pulmonary fibrosis (PF), especially idiopathic pulmonary fibrosis (IPF), is a chronic lung disease that lacks a proven effective therapy. The present study evaluated the therapeutic effect of PTL on PF. METHODS: Serum-starved primary lung fibroblasts and HFL1 cells were treated with different doses of PTL, and cell viability and the migration rate were measured. Western blot analysis and a dual-luciferase assay were used to analyze the epithelial-mesenchymal transition (EMT)-related transcription factors influenced by PTL treatment in A549 cells and primary lung epithelial cells. Mice with bleomycin (BLM)-induced pulmonary fibrosis were treated with different doses of intragastric PTL, and pathological changes were evaluated using Hematoxylin-eosin (H&E) staining and immunohistochemical analysis. RESULTS: Our results demonstrated that PTL reduced the cell viability and migration rate of lung fibroblasts and inhibited the expression of EMT-related transcription factors in lung epithelial cells. In vivo studies demonstrated that PTL attenuated BLM-induced pulmonary fibrosis and improved the body weight and pathological changes of BLM-treated mice. We further demonstrated that PTL attenuated BLM-induced PF primarily via inhibition of the NF-κB/Snail signaling pathway. CONCLUSION: These findings suggest that PTL inhibits EMT and attenuates BLM-induced PF via the NF-κB/Snail signaling pathway. PTL is a worthwhile candidate compound for pulmonary fibrosis therapy.

Isolation and identification of polyphenols from Marsilea quadrifolia with antioxidant properties in vitro and in vivo.

Marsilea quadrifolia is an edible aquatic medicinal plant used as a traditional health food in Asia. Four new polyphenols including kaempferol 3-O-(2″-O-E-caffeoyl)-ß-d-glucopyranoside (1), kaempferol 3-O-(3″-O-E-caffeoyl)-α-l-arabinopyranoside (3), 4-methy-3'-hydroxypsilotinin (4) and (±)-(E)-4b-methoxy-3b,5b-dihydroxyscirpusin A (18) together with 14 known ones (2, 5-17) were isolated from the ethanol extract of M. quadrifolia. Structures of the new compounds were elucidated by extensive spectroscopic analyses. In DPPH and oxygen radical absorbance capacity antioxidant assays, some compounds showed stronger antioxidant activities and quercetin (9) was the most potent antioxidant in both assays. In a restraint-induced oxidative stress model in mice, quercetin significantly attenuated the increase in plasma ALT and AST levels as well as liver MDA content of restrained mice. Liver SOD activity was also significantly increased by quercetin, indicating a significant in vivo antioxidant activity. As a rich source of polyphenols with strong antioxidant activities, M. quadrifolia may be developed to a product for relieving oxidative stress.