Effects of capsaicin treatment on immunoglobulin secretion in the rat: further evidence for involvement of tachykinin-containing afferent nerves

Eglezos, Anthony; Andrews, Paul V.; Boyd, Richard; Helme, Robert D.

doi:10.1016/0165-5728(90)90084-z

Cited by 39 publications

(13 citation statements)

References 31 publications

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“…But, as for ROS generation, this occurs only in activated or transformed lymphoid cells. In neuronal cells, capsaicin provokes the uptake of external 45 Ca 2+ , which can be inhibited by ruthenium red (a calcium channel blocker), concluding that in these cells calcium mobilization is mainly of extracellular origin (see revision of Holzer: 34 ). However, in lymphoid cells, our results with BAPTA-AM and EGTA have demonstrated that capsaicin mediates the uptake of extracellular calcium and mobilizes the intracellular`pools' of calcium.…”

Section: Discussionmentioning

confidence: 99%

Selective induction of apoptosis by capsaicin in transformed cells: the role of reactive oxygen species and calcium

et al. 1999

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Capsaicin is a vanilloid quinone analog that inhibits the plasma membrane electron transport (PMOR) system and induces apoptosis in transformed cells. Using a cytofluorimetric approach we have determined that capsaicin induces a rapid increase of reactive oxygen species (ROS) followed by a subsequent disruption of the transmembrane mitochondrial potential (DC m ) and DNA nuclear loss in transformed cell lines and in mitogen activated human T cells. This apoptotic pathway is biochemically different from the typical one induced by either ceramide or edelfosine where, in our system, the DC m dissipation precedes the generation of reactive oxygen species. Neither production of ROS nor apoptosis was found in capsaicin-treated resting T cells where the activity of the PMOR system is minimal when compared with mitogen activated or transformed T cells. Capsaicin also induces Ca 2+ mobilization in activated but not in resting T cells. However, preincubation of cells with BAPTA-AM, which chelate cytosolic free calcium, did not prevent ROS generation or apoptosis induced by capsaicin, suggesting that ROS generation in capsaicin treated cells is not a consequence of calcium signaling and that the apoptotic pathway may be separated from the one that mobilizes calcium. Moreover, we present data for the implication of a possible vanilloid receptor in calcium mobilization, but not in ROS generation. These results provide evidence that the PMOR system may be an interesting target to design antitumoral and anti-inflammatory drugs.

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Section: Discussionmentioning

confidence: 99%

Selective induction of apoptosis by capsaicin in transformed cells: the role of reactive oxygen species and calcium

et al. 1999

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“…Both and d opioid receptors have been located on primary afferent sensory nerves [24,25] and these receptors could be mediating the inhibitory effect of hemorphin-7. It is unlikely that opioid receptors on immunocytes are involved in the action of hemorphin-7 in our experiments, as migration of these cells to the site of tissue injury does not occur until the late phase of acute inflammation (about 5-6 h after blister induction) [26,27].…”

Section: Discussionmentioning

confidence: 76%

Modulation of peripheral inflammation by locally administered hemorphin-7

1998

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The results of this study suggest that hemorphins might play a role in inhibiting the inflammatory response in acute, but not in recurrent or chronic injury conditions. Evidence is also provided that the modulatory inhibitory effect of hemorphin-7 is mediated via activation of opioid receptor(s). The significance of this study in conjunction with our previous work, is that it raises the possibility that different endogenous inhibitory mechanisms may operate under different injury conditions - endogenous hemorphins and opioids may modulate acute and chronic inflammation, respectively.

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“…In other model systems, however, b-funaltrexamine, an irreversible m-selective antagonist, have fully reversed the actions of endomorphins [9] suggesting the involvement of m-receptors. It is unlikely that opioid receptors on immunocytes are involved in the action of EM-1 in our experiment, as migration of these cells to the site of tissue injury does not occur until the late phase of acute inflammation (about 5-6 h after blister induction) [28,29].…”

Section: Discussionmentioning

confidence: 81%

Modulation of peripheral inflammation by locally administered endomorphin-1

Khalil¹,

Sanderson

Modig

et al. 1999

Inflammation Research

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The current results demonstrate a greater inhibitory effect of EM-1 on the inflammatory response to electrical nerve stimulation (58% inhibition) compared to SP (34% inhibition) suggesting the involvement of both pre- and post-terminal mechanisms in the inhibitory modulatory actions of EM-1. Evidence is provided for the involvement of opioid receptors in this inhibitory effect. The results also suggest that EM-1 is equipotent in inhibiting the inflammatory response under different injury conditions.

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Effects of capsaicin treatment on immunoglobulin secretion in the rat: further evidence for involvement of tachykinin-containing afferent nerves

Cited by 39 publications

References 31 publications

Selective induction of apoptosis by capsaicin in transformed cells: the role of reactive oxygen species and calcium

Selective induction of apoptosis by capsaicin in transformed cells: the role of reactive oxygen species and calcium

Modulation of peripheral inflammation by locally administered hemorphin-7

Modulation of peripheral inflammation by locally administered endomorphin-1

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