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A β-D-glucan was obtained from the edible mushroom Pholiota nameko by hot aqueous extraction and purification. NMR and methylation analyses of the purified fraction (GHW-PN, 1.46% yield) indicated the presence of a (1 → 3)-linked β-D-glucan, highly substituted (~27%) at O-6 by single units of β-D-Glcp or by (1 → 6)-β-D-Glcp fragments. The β-glucan (at 0.5, 1, and 2%) showed shear thinning behavior and when the concentration of the solution increased, there was an increase in apparent viscosity. The β-D-glucan presented gel-like behavior and thermal stability under a simulated pasteurization process, suggesting its potential as a thickening and gelling agent in products submitted to temperature variations. The β-D-glucan at 0.3, 1.0 and 3.0 mg kg significantly inhibited the inflammatory pain in 24.8, 56.9 and 82.3%, respectively, in the formalin-induced nociception in mice. The results pointed out that the β-D-glucan (GHW-PN) isolated from P. nameko presents potential application for the food industry or for medical purposes.

Aims:The covalent linking of nonsteroidal anti-inflammatory drugs to a hydrogen sulfide (H 2 S)-releasing moiety has been shown to dramatically reduce gastrointestinal (GI) damage and bleeding, as well as increase anti-inflammatory and analgesic potency. We have tested the hypothesis that an H 2 S-releasing derivative of ketoprofen (ATB-352) would exhibit enhanced efficacy without significant GI damage in a mouse model of allodynia/hyperalgesia. Results: ATB-352 was significantly more potent and effective as an analgesic than ketoprofen and did not elicit GI damage. Pretreatment with an antagonist of the CB1 cannabinoid receptor (AM251) significantly reduced the analgesic effects of ATB-352. The CB1 antagonist exacerbated GI damage when coadministered with ketoprofen, but GI damage was not induced by the combination of ATB-352 and the CB1 antagonist. In vitro, ATB-352 was substantially more potent than ketoprofen as an inhibitor of fatty acid amide hydrolase, consistent with a contribution of endogenous cannabinoids to the analgesic effects of this drug. Blood anandamide levels were significantly depressed by ketoprofen, but remained unchanged after treatment with ATB-352. Innovation: Ketoprofen is a potent analgesic, but its clinical use, even in the short term, is significantly limited by its propensity to cause significant ulceration and bleeding in the GI tract. Covalently linking an H 2 S-releasing moiety to ketoprofen profoundly reduces the GI toxicity of the drug, while boosting analgesic effectiveness. Conclusion: This study demonstrates a marked enhancement of the potency and effectiveness of ATB-352, an H 2 S-releasing derivative of ketoprofen, in part, through the involvement of the endogenous cannabinoid system. This may have significant advantages for the control and management of pain, such as in a postoperative setting.

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