Abstract
Cigarette smoking is a major prodromal factor for the onset of many adverse health effects that may occur in the short run and is the leading cause of preventable disease, disability, and death in the United States. Moreover, it is well established that chronic smoking is associated with vascular endothelial dysfunction in a causative and dose-dependent manner primarily related to the release of reactive oxygen species (ROS), nicotine, and the induction of oxidative stress (OS)-driven inflammation. Preclinical studies have also shown that nicotine (the principal e-liquid ingredient used in e-cigarettes) can also cause OS, exacerbating cerebral ischemia and secondary brain injury. Likewise, chronic e-Cig va** could be prodromal to cerebrovascular impairment and promote cerebrovascular conditions favoring stroke onset and worsening post-ischemic brain injury. Therefore, using mouse models is crucial to understand how xenobiotics such as those released by conventional and/or e-cigs can impact the onset and severity of stroke as well as post-stroke recovery. To appropriately model human-like smoking/va** behavior in mice, however, the exposure to these xenobiotics must be standardized and undertaken in a controlled environment. This chapter describes a well-validated protocol to reproduce standardized chronic tobacco smoke or e-cigarette vape exposure in mice in the setting of a mouse transient ischemic stroke model.
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Acknowledgments
This work was supported by the National Institutes of Health/National Institute on Drug Abuse 2R01-DA029121 and 1R01-DA049737 and the National Institute of Neurological Disorders and Stroke 1R01NS117906 to Dr. Luca Cucullo.
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Mancuso, S., Bhalerao, A., Cucullo, L. (2023). Use of Conventional Cigarette Smoking and E-Cigarette Va** for Experimental Stroke Studies in Mice. In: Karamyan, V.T., Stowe, A.M. (eds) Neural Repair. Methods in Molecular Biology, vol 2616. Humana, New York, NY. https://doi.org/10.1007/978-1-0716-2926-0_31
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DOI: https://doi.org/10.1007/978-1-0716-2926-0_31
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