Tempo Regular Menthol Tissues x 1

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In first aid products such as "mineral ice" to produce a cooling effect as a substitute for real ice in the absence of water or electricity (pouch, body patch/sleeve or cream). The estimated lethal dose for menthol (and peppermint oil) in humans may be as low as 50–500mg/kg, (LD50 Acute: 3300mg/kg [Rat]. 3400mg/kg [Mouse]. 800mg/kg [Cat]). Results: The decrease in pro-inflammatory cytokines and related inflammatory markers, as well as associated pathway activation, was found to play the greatest role in the protective effects of menthol against inflammatory damage or association with protection against chronic inflammation.

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The photography was performed in the Histology and Cell Biology Department, Faculty of Medicine, Minia University. An Olympus (U.TV0.5XC-3) light microscope with a digital camera was used in this experiment. Photomicrographs were assessed by Adobe Photoshop. Morphometric Study for Management of Science and Technology Development, Ton Duc Thang University, Ho Chi Minh City, Vietnam James A. Duke (2002), "PEPPERMINT", Handbook of Medicinal Herbs (2nded.), pp.562–564, ISBN 978-0-8493-1284-7In the natural compound, the isopropyl group is in the trans orientation to both the methyl and hydroxyl groups. Thus, it can be drawn in any of the ways shown: Menthol has demonstrated anti-inflammatory effects within the gastric mucosa in an experimental model of ethanol-induced gastric ulcers ( 37). Ethanol-induced gastric ulcers are characterized by marked inflammatory responses following the generation of reactive oxygen species and a vigorous immune reaction ( 48). The study found that menthol administration led to an increase in anti-inflammatory interleukin (IL)-10 expression, while there was a reduction in pro-inflammatory markers, including IL-6 and tumor necrosis factor-α (TNF-α). The changes in these inflammatory markers were all statistically significant compared with baseline levels (P<0.001). This study investigated the antioxidant, anti-apoptotic, and anti-inflammatory effects of menthol, providing the potential to differentiate these effects within a model whereby all three factors contribute to ulceration and associated symptoms ( 37). Importantly, menthol administration led to a reduction in markers of antioxidant activity and a reduction in the neutrophilic immune response in the gastric mucosa, which collectively suggests a gastroprotective effect. Jerrold B. Leikin; Frank P. Paloucek, eds. (2008), "Peppermint Oil", Poisoning and Toxicology Handbook (4thed.), Informa, p.885, ISBN 978-1-4200-4479-9

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Another hypothesis is that perfusion decrease may be attributed to a decrease in tissue/organ temperature, not in response to menthol but rather to the ethanol contained in the formulation. In recent studies, topical menthol application caused a decrease in muscle ( Hunter et al., 2018) and skin temperature ( Lasanen et al., 2016), irrespective of concentration. In both cases this response was not attributed to a possible menthol action on the vasculature (not measured) but rather to an increase in evaporative heat loss caused by ethanol ( Hunter et al., 2018), which may have directly caused vessel constriction. This again suggests that menthol permeation of muscle from topical application is not likely to occur. Again, it is also possible that ethanol interfered with TRPM8 channels, decreasing menthol activity, a hypothesis that needs further investigation. A macro photograph of menthol crystals Menthol crystals at room temperature. Approx. 1cm in length.Despite the uncertainty over the value of topical menthol in reducing inflammation that is established in the skin, the anti-inflammatory effects of menthol have been proposed to influence wound healing, as investigated by Rozza et al. ( 61). Skin wound healing is a complex process that includes an inflammatory phase, whereby reductions in inflammatory markers, including IL-6, have been linked to accelerated skin wound healing ( 61). In this study, the authors evaluated the effects of different periods of time of treatment with menthol (3, 7, or 14 days) in rats with skin wounds, comparing collagenase-based and menthol-based creams. The menthol-based cream led to accelerated healing within the first three days of treatment, which is consistent with a reduction in the initial inflammatory phase of wound healing when compared with collagenase-based creams. Furthermore, this healing was linked to a reduction in pro-inflammatory cytokines TNF-α and IL-6 (reduced expression of mRNA). Over time, menthol-based treatment was found to not only decrease pro-inflammatory cytokine levels through the inflammatory, proliferative, and remodeling phases of wound healing. Menthol's ability to chemically trigger the cold-sensitive TRPM8 receptors in the skin is responsible for the well-known cooling sensation it provokes when inhaled, eaten, or applied to the skin. [3] In this sense, it is similar to capsaicin, the chemical responsible for the spiciness of hot chilis (which stimulates heat sensors, also without causing an actual change in temperature). Sepsis is a complex and serious complication in postoperative critical care patients, mainly because of infection. It is a major cause of ICU patient morbidity as well as mortality ( 1, 2). The condition is characterized by multiple organ damage, with the kidneys and the lungs being the most vulnerable organs ( 3). About 50% of patients with sepsis may experience acute kidney (AKI) and lung injuries (ALI). Despite all improved and labored treatment strategies to medicate sepsis patients, the mortality rate for patients with AKI and ALI is at alarming levels (up to 70%) ( 4, 5). Thus, the research aiming to identify novel therapies and prevention approaches, which should be both effective and safe, is a pressing need for sepsis management.

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In nonprescription products for short-term relief of minor sore throat and minor mouth or throat irritation e.g.: lip balms and cough medicines.Key Findings: A survival study showed that menthol enhanced the survival after sepsis from 0% in septic group to 30%. Septic rats developed histological evidence of ALI and AKI. Menthol markedly suppressed sepsis induced elevation of tissue TNF-a, ameliorated sepsis-induced cleavage of caspase-3 and restored the antiapoptotic marker Bcl2. Henderson, B. J.; Wall, T. R.; Henley, B. M.; Kim, C. H.; Nichols, W. A.; Moaddel, R.; Xiao, C.; Lester, H. A. (2016). "Menthol Alone Upregulates Midbrain nAChRs, Alters nAChR Subtype Stoichiometry, Alters Dopamine Neuron Firing Frequency, and Prevents Nicotine Reward". J. Neurosci. 36 (10): 2957–2974. doi: 10.1523/JNEUROSCI.4194-15.2016. PMC 4783498. PMID 26961950.