“…Utilized by millions of individuals globally, Vicks VapoRub * has been a household name for over a century, being advocated for its use in managing the symptoms associated with mild upper respiratory tract infections (URTIs). [1][2][3] The main constituents of Vicks VapoRub are menthol, camphor, eucalyptus oil and turpentine oil in a petrolatum base. [4][5][6][7] It is worth noting that menthol, camphor and eucalyptus oil also form the main ingredients in numerous other cough and cold remedies and have therefore been the focus of a number of studies.…”
Background
Over-the-counter therapies, such as Vicks VapoRub, are frequently used in the management of upper respiratory tract infection symptoms. Of these, acute cough is the most bothersome; however, the mechanisms involved have not been fully elucidated. The temperature-sensitive transient receptor potential (TRP) channels, including TRPA1, TRPV1, TRPM8 and TRPV4, are potential candidates. TRPV4 is also thought to be involved in cough through the TRPV4–ATP–P2X3 pathway. Here, we hypothesise that Vicks VapoRub ingredients (VVRIs) modulate the TRP cough channels.
Methods
Stably transfected HEK cells expressing TRP channels were challenged with VVRIs, individually or in combination, and the agonist and antagonist effects were measured using calcium signalling responses. In addition, rhinovirus serotype-16 (RV16)-infected A549 airway epithelial cells were pre-incubated with individual or combinations of VVRIs prior to hypotonic challenge and extracellular ATP release analysis.
Results
Calcium signalling reconfirmed some previously defined activation of TRP channels by specific VVRIs. The combined VVRIs containing menthol, camphor and eucalyptus oil activated TRPV1, TRPV4, TRPM8 and untransfected wild-type HEK293 cells. However, pre-incubation with VVRIs did not significantly inhibit any of the channels compared with the standard agonist responses. Pre-incubation of RV16-infected A549 cells with individual or combined VVRIs, except menthol, resulted in a 0.45–0.55-fold reduction in total ATP release following hypotonic stimulation, compared with infected cells not treated with VVRIs.
Conclusion
These findings suggest that some VVRIs may reduce symptoms associated with upper respiratory tract infection by modulating specific TRP receptors and by reducing RV16-induced ATP release.
“…Utilized by millions of individuals globally, Vicks VapoRub * has been a household name for over a century, being advocated for its use in managing the symptoms associated with mild upper respiratory tract infections (URTIs). [1][2][3] The main constituents of Vicks VapoRub are menthol, camphor, eucalyptus oil and turpentine oil in a petrolatum base. [4][5][6][7] It is worth noting that menthol, camphor and eucalyptus oil also form the main ingredients in numerous other cough and cold remedies and have therefore been the focus of a number of studies.…”
Background
Over-the-counter therapies, such as Vicks VapoRub, are frequently used in the management of upper respiratory tract infection symptoms. Of these, acute cough is the most bothersome; however, the mechanisms involved have not been fully elucidated. The temperature-sensitive transient receptor potential (TRP) channels, including TRPA1, TRPV1, TRPM8 and TRPV4, are potential candidates. TRPV4 is also thought to be involved in cough through the TRPV4–ATP–P2X3 pathway. Here, we hypothesise that Vicks VapoRub ingredients (VVRIs) modulate the TRP cough channels.
Methods
Stably transfected HEK cells expressing TRP channels were challenged with VVRIs, individually or in combination, and the agonist and antagonist effects were measured using calcium signalling responses. In addition, rhinovirus serotype-16 (RV16)-infected A549 airway epithelial cells were pre-incubated with individual or combinations of VVRIs prior to hypotonic challenge and extracellular ATP release analysis.
Results
Calcium signalling reconfirmed some previously defined activation of TRP channels by specific VVRIs. The combined VVRIs containing menthol, camphor and eucalyptus oil activated TRPV1, TRPV4, TRPM8 and untransfected wild-type HEK293 cells. However, pre-incubation with VVRIs did not significantly inhibit any of the channels compared with the standard agonist responses. Pre-incubation of RV16-infected A549 cells with individual or combined VVRIs, except menthol, resulted in a 0.45–0.55-fold reduction in total ATP release following hypotonic stimulation, compared with infected cells not treated with VVRIs.
Conclusion
These findings suggest that some VVRIs may reduce symptoms associated with upper respiratory tract infection by modulating specific TRP receptors and by reducing RV16-induced ATP release.
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