Topical Capsaicin in Dermatologic and Peripheral Pain Disorders

Rumsfield, Jean; West, Dennis P.

doi:10.1177/106002809102500409

Cited by 73 publications

(44 citation statements)

References 28 publications

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“…The reported indicated that the intake of capsaicin in a typical Indian or Thai diet was about 128 µg/kg human body weight (44). The concentrations of capsaicin in the gastric fluid (1-3 L) would be equivalent to 8-25 µM for an adult human with a body weight of 60 kg.…”

Section: Discussionmentioning

confidence: 99%

Effects of Capsaicin on Induction of Apoptosis and Inhibition of Adipogenesis in 3T3-L1 Cells

Hsu

Yen

2007

J. Agric. Food Chem.

185

129

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Currently, at the beginning of the 21st century, obesity has become the leading metabolic disease in the world. It is a serious health problem in industrialized countries. Previous research has suggested that decreased preadipocyte differentiation and proliferation and decreased lipogenesis are mechanisms to reduce obesity. In the present study, the effects of capsaicin on the induction of apoptosis and inhibition of lipid accumulation in 3T3-L1 preadipocytes and adipocytes were investigated. The results demonstrated that capsaicin decreased cell population growth of 3T3-L1 preadipocytes, assessed with the MTT assay. Flow cytometric analysis of 3T3-L1 preadipocytes exposed to capsaicin showed that apoptotic cells increased in a time-and dose-dependent manner. Treatment with capsaicin decreased the number of normal cells and increased the number of early apoptotic and late apoptotic cells in a dose-dependent manner. The treatment of cells with capsaicin caused the loss of mitochondria membrane potential (∆Ψm). The induction of apoptosis in 3T3-L1 preadipocytes by capsaicin was mediated through the activation of caspase-3, Bax, and Bak, and then through the cleavage of PARP and the down-regulation of Bcl-2. Moreover, capsaicin significantly decreased the amount of intracellular triglycerides and glycerol-3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 adipocytes. Capsaicin also inhibited the expression of PPARγ, C/EBPR, and leptin, but induced up-regulation of adiponectin at the protein level. These results demonstrate that capsaicin efficiently induces apoptosis and inhibits adipogenesis in 3T3-L1 preadipocytes and adipocytes.

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Section: Discussionmentioning

confidence: 99%

Effects of Capsaicin on Induction of Apoptosis and Inhibition of Adipogenesis in 3T3-L1 Cells

Hsu

Yen

2007

J. Agric. Food Chem.

185

129

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“…The desensitizing effect of channel activation has been utilized clinically to reduce the afferent transmission of painful stimuli (27). Repeated activation of TRPV1 by chemical stimuli results in calcium-dependent desensitization of the receptor (24).…”

mentioning

confidence: 99%

Cannabinoid WIN 55,212-2 Regulates TRPV1 Phosphorylation in Sensory Neurons

Jeske

Patwardhan

Gamper

et al. 2006

Journal of Biological Chemistry

133

131

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Cannabinoids are known to have multiple sites of action in the nociceptive system, leading to reduced pain sensation. However, the peripheral mechanism(s) by which this phenomenon occurs remains an issue that has yet to be resolved. Because phosphorylation of TRPV1 (transient receptor potential subtype V1) plays a key role in the induction of thermal hyperalgesia in inflammatory pain models, we evaluated whether the cannabinoid agonist WIN 55,212-2 (WIN) regulates the phosphorylation state of TRPV1. Here, we show that treatment of primary rat trigeminal ganglion cultures with WIN led to dephosphorylation of TRPV1, specifically at threonine residues. Utilizing Chinese hamster ovary cell lines, we demonstrate that Thr 144 and Thr 370 were dephosphorylated, leading to desensitization of the TRPV1 receptor. This post-translational modification occurred through activation of the phosphatase calcineurin (protein phosphatase 2B) following WIN treatment. Furthermore, knockdown of TRPA1 (transient receptor potential subtype A1) expression in sensory neurons by specific small interfering RNA abolished the WIN effect on TRPV1 dephosphorylation, suggesting that WIN acts through TRPA1. We also confirm the importance of TRPA1 in WIN-induced dephosphorylation of TRPV1 in Chinese hamster ovary cells through targeted expression of one or both receptor channels. These results imply that the cannabinoid WIN modulates the sensitivity of sensory neurons to TRPV1 activation by altering receptor phosphorylation. In addition, our data could serve as a useful strategy in determining the potential use of certain cannabinoids as peripheral analgesics.Cannabinoids have been shown to exert anti-inflammatory and anti-hyperalgesic effects via peripheral site(s) of action in several pain models (1-5). These effects are thought to be mediated by cannabinoid type 1 (CB1) 4 and/or 2 (CB2) receptor activation, both peripherally and centrally (4 -7). Cannabinoids could exert their effects by acting on CB1/CB2 receptors located on sensory neurons and/or other peripheral cells influencing sensory neuronal function (8). However, there is a Ͻ5-10% co-localization of metabotropic CB1/CB2 receptors with nociceptive neuronal markers such as TRPV1 (transient receptor potential subtype V1) and calcitonin gene-related peptide in trigeminal and dorsal root ganglion neurons (9 -11), suggesting that cannabinoids could act on nociceptors through non-CB1/CB2 receptor mechanism(s). Certain cannabinoids have been shown to activate channels such as TRPV1, including arachidonyl-2-chloroethylamide (ACEA) (12), N-arachidonoyldopamine (13), and anandamide (14), as well as TRPA1 (transient receptor potential subtype A1), including ⌬ 9 -tetrahydrocannabinol (15). In addition, the synthetic cannabinoid R(ϩ)-WIN 55,212-2 (WIN) has demonstrated non-CB1/CB2 receptor activities in trigeminal ganglia (11). The results from these studies suggest that cannabinoids may activate calcium channel function similar to non-cannabinoid transient receptor potential agonists, including the...

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“…OC for defense formulas can vary in potency fiom 16,000 Scoville Heat Units (S.H.U.) to 1.5 million units, with a 5-10% solution generally recommended as an effective dose (13). However, because OC is inflammatory as well as irritating, increasing the strength also increases the safety risks.…”

Section: Olmrcsin Capsicummentioning

confidence: 99%

Oleoresin Capsicum toxicology evaluation and hazard review

Archuleta¹

1995

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Topical Capsaicin in Dermatologic and Peripheral Pain Disorders

Cited by 73 publications

References 28 publications

Effects of Capsaicin on Induction of Apoptosis and Inhibition of Adipogenesis in 3T3-L1 Cells

Effects of Capsaicin on Induction of Apoptosis and Inhibition of Adipogenesis in 3T3-L1 Cells

Cannabinoid WIN 55,212-2 Regulates TRPV1 Phosphorylation in Sensory Neurons

Oleoresin Capsicum toxicology evaluation and hazard review

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