The purpose of this research is to develop an effective and inexpensive oxygen evolution reaction (OER) electrocatalyst to achieve high-efficiency water decomposition. Herein, Keggin-type polyoxometalate (POM) nanoparticles coated with zeolitic imidazolate framework (ZIF-67) were successfully synthesized by facile methods. An efficient ZIF-67@POM catalyst with yolk/shell structure is reported. The POM nanomaterials are uniformly dispersed in the surface of ZIF-67. This unique yolk/shell structure with potential synergistic interaction between POM and ZIF-67 results in superior electrocatalytic activity in OER. When the current density is 10 mA cm–2, the overpotential is only 287 mV, and the Tafel slope is 58 mV per decade. Moreover, the as-prepared yolk/shell ZIF-67@POM catalysts exhibit excellent cycling stability, high surface area, abundant surface active sites, and high diffusion efficiency comparable to the traditional noble-metal-free OER electrocatalyst.

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Stress ulceration is a common complication in critically ill patients and can result in significant upper gastrointestinal bleeding associated with a high morbidity and mortality. At present, little is known of the molecular mechanisms underlying the incidence of this type of gastric damage. In the present study, we investigated the temporal activation of the redox-sensitive p38 signaling transduction cascade and its roles in a well-defined experimental model of cold immobilization stress-induced gastric ulceration. Exposure of Sprague-Dawley rats to 6 h of cold immobilization stress led to a rapid activation of p38 in the gastric mucosa at as early as 15 min after stress, and this activation was maximal after 1.5 h of stress and still persisted until the end of stress. Selectively blocking p38 by pretreatment with SB 239063, a potent and selective p38 inhibitor, suppressed the stress-promoted TNF-α, IL-1β, and CINC-1 production and then prevented the subsequent neutrophil infiltration, gastric mucosal epithelial necrosis and apoptosis, and the ulcerative lesions formation. Prior administration of the free radical scavengers, tempol and N-acetyl-l-cysteine, abolished the stress induction of p38 activation and the resulting mucosal inflammation and gastric injury. These results demonstrate that reactive oxygen species-mediated p38 activation plays an essential role in the pathogenesis of stress-induced gastric inflammatory damage in the rat model of cold immobilization stress. Our findings suggested that inhibition of p38 activation might be a potential strategy for the prophylaxis and treatment of stress ulceration.