Tags

Type your tag names separated by a space and hit enter

Possible involvement of peripheral TRP channels in the hydrogen sulfide-induced hyperalgesia in diabetic rats.
BMC Neurosci. 2019 Jan 03; 20(1):1.BN

Abstract

BACKGROUND

Peripheral diabetic neuropathy can be painful and its symptoms include hyperalgesia, allodynia and spontaneous pain. Hydrogen sulfide (H2S) is involved in diabetes-induced hyperalgesia and allodynia. However, the molecular target through which H2S induces hyperalgesia in diabetic animals is unclear. The aim of this study was to determine the possible involvement of transient receptor potential (TRP) channels in H2S-induced hyperalgesia in diabetic rats.

RESULTS

Streptozotocin (STZ) injection produced hyperglycemia in rats. Intraplantar injection of NaHS (an exogenous donor of H2S, 3-100 µg/paw) induced hyperalgesia, in a time-dependent manner, in formalin-treated diabetic rats. NaHS-induced hyperalgesia was partially prevented by local intraplantar injection of capsazepine (0.3-3 µg/paw), HC-030031 (100-316 µg/paw) and SKF-96365 (10-30 µg/paw) blockers, at 21 days post-STZ injection. At the doses used, these blockers did not modify formalin-induced nociception. Moreover, capsazepine (0.3-30 µg/paw), HC-030031 (100-1000 µg/paw) and SKF-96365 (10-100 µg/paw) reduced formalin-induced nociception in diabetic rats. Contralateral injection of the highest doses used did not modify formalin-induced flinching behavior. Hyperglycemia, at 21 days, also increased protein expression of cystathionine-β-synthase enzyme (CBS) and TRPC6, but not TRPA1 nor TRPV1, channels in dorsal root ganglia (DRG). Repeated injection of NaHS enhanced CBS and TRPC6 expression, but hydroxylamine (HA) prevented the STZ-induced increase of CBS protein. In addition, daily administration of SKF-96365 diminished TRPC6 protein expression, whereas NaHS partially prevented the decrease of SKF-96365-induced TRPC6 expression. Concordantly, daily intraplantar injection of NaHS enhanced, and HA prevented STZ-induced intraepidermal fiber loss, respectively. CBS was expressed in small- and medium-sized cells of DRG and co-localized with TRPV1, TRPA1 and TRPC6 in IB4-positive neurons.

CONCLUSIONS

Our data suggest that H2S leads to hyperalgesia in diabetic rats through activation of TRPV1, TRPA1 and TRPC channels and, subsequent intraepidermal fibers loss. CBS enzyme inhibitors or TRP-channel blockers could be useful for treatment of painful diabetic neuropathy.

Authors+Show Affiliations

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón s/n, Col. Casco de Santo Tomas, Miguel Hidalgo, 11340, Ciudad de México, Mexico.Neurobiology of Pain Laboratory, Departamento de Farmacobiología, Cinvestav, Unidad Coapa, Calzada de los Tenorios 235, Col. Granjas Coapa, 14330, Ciudad de México, Mexico.Neurobiology of Pain Laboratory, Departamento de Farmacobiología, Cinvestav, Unidad Coapa, Calzada de los Tenorios 235, Col. Granjas Coapa, 14330, Ciudad de México, Mexico.Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón s/n, Col. Casco de Santo Tomas, Miguel Hidalgo, 11340, Ciudad de México, Mexico.Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón s/n, Col. Casco de Santo Tomas, Miguel Hidalgo, 11340, Ciudad de México, Mexico.Unidad de Investigación en Farmacología, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Secretaría de Salud, Calzada de Tlalpan 4502, Col. Sección XVI, Tlalpan, 14080, Ciudad de México, Mexico.Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón s/n, Col. Casco de Santo Tomas, Miguel Hidalgo, 11340, Ciudad de México, Mexico.Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón s/n, Col. Casco de Santo Tomas, Miguel Hidalgo, 11340, Ciudad de México, Mexico. Unidad de Investigación en Farmacología, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas", Secretaría de Salud, Calzada de Tlalpan 4502, Col. Sección XVI, Tlalpan, 14080, Ciudad de México, Mexico.Neurobiology of Pain Laboratory, Departamento de Farmacobiología, Cinvestav, Unidad Coapa, Calzada de los Tenorios 235, Col. Granjas Coapa, 14330, Ciudad de México, Mexico.Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón s/n, Col. Casco de Santo Tomas, Miguel Hidalgo, 11340, Ciudad de México, Mexico. hector.isaac@gmail.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30602386

Citation

Roa-Coria, José Eduardo, et al. "Possible Involvement of Peripheral TRP Channels in the Hydrogen Sulfide-induced Hyperalgesia in Diabetic Rats." BMC Neuroscience, vol. 20, no. 1, 2019, p. 1.
Roa-Coria JE, Pineda-Farias JB, Barragán-Iglesias P, et al. Possible involvement of peripheral TRP channels in the hydrogen sulfide-induced hyperalgesia in diabetic rats. BMC Neurosci. 2019;20(1):1.
Roa-Coria, J. E., Pineda-Farias, J. B., Barragán-Iglesias, P., Quiñonez-Bastidas, G. N., Zúñiga-Romero, Á., Huerta-Cruz, J. C., Reyes-García, J. G., Flores-Murrieta, F. J., Granados-Soto, V., & Rocha-González, H. I. (2019). Possible involvement of peripheral TRP channels in the hydrogen sulfide-induced hyperalgesia in diabetic rats. BMC Neuroscience, 20(1), 1. https://doi.org/10.1186/s12868-018-0483-3
Roa-Coria JE, et al. Possible Involvement of Peripheral TRP Channels in the Hydrogen Sulfide-induced Hyperalgesia in Diabetic Rats. BMC Neurosci. 2019 Jan 3;20(1):1. PubMed PMID: 30602386.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible involvement of peripheral TRP channels in the hydrogen sulfide-induced hyperalgesia in diabetic rats. AU - Roa-Coria,José Eduardo, AU - Pineda-Farias,Jorge Baruch, AU - Barragán-Iglesias,Paulino, AU - Quiñonez-Bastidas,Geovanna Nallely, AU - Zúñiga-Romero,Ángel, AU - Huerta-Cruz,Juan Carlos, AU - Reyes-García,Juan Gerardo, AU - Flores-Murrieta,Francisco Javier, AU - Granados-Soto,Vinicio, AU - Rocha-González,Héctor Isaac, Y1 - 2019/01/03/ PY - 2018/04/18/received PY - 2018/12/20/accepted PY - 2019/1/4/entrez PY - 2019/1/4/pubmed PY - 2019/8/16/medline KW - Cystathionine-β-synthase KW - Hydrogen sulfide KW - Hyperalgesia KW - Painful diabetic peripheral neuropathy KW - Streptozotocin-induced diabetes KW - Transient receptor potential channels SP - 1 EP - 1 JF - BMC neuroscience JO - BMC Neurosci VL - 20 IS - 1 N2 - BACKGROUND: Peripheral diabetic neuropathy can be painful and its symptoms include hyperalgesia, allodynia and spontaneous pain. Hydrogen sulfide (H2S) is involved in diabetes-induced hyperalgesia and allodynia. However, the molecular target through which H2S induces hyperalgesia in diabetic animals is unclear. The aim of this study was to determine the possible involvement of transient receptor potential (TRP) channels in H2S-induced hyperalgesia in diabetic rats. RESULTS: Streptozotocin (STZ) injection produced hyperglycemia in rats. Intraplantar injection of NaHS (an exogenous donor of H2S, 3-100 µg/paw) induced hyperalgesia, in a time-dependent manner, in formalin-treated diabetic rats. NaHS-induced hyperalgesia was partially prevented by local intraplantar injection of capsazepine (0.3-3 µg/paw), HC-030031 (100-316 µg/paw) and SKF-96365 (10-30 µg/paw) blockers, at 21 days post-STZ injection. At the doses used, these blockers did not modify formalin-induced nociception. Moreover, capsazepine (0.3-30 µg/paw), HC-030031 (100-1000 µg/paw) and SKF-96365 (10-100 µg/paw) reduced formalin-induced nociception in diabetic rats. Contralateral injection of the highest doses used did not modify formalin-induced flinching behavior. Hyperglycemia, at 21 days, also increased protein expression of cystathionine-β-synthase enzyme (CBS) and TRPC6, but not TRPA1 nor TRPV1, channels in dorsal root ganglia (DRG). Repeated injection of NaHS enhanced CBS and TRPC6 expression, but hydroxylamine (HA) prevented the STZ-induced increase of CBS protein. In addition, daily administration of SKF-96365 diminished TRPC6 protein expression, whereas NaHS partially prevented the decrease of SKF-96365-induced TRPC6 expression. Concordantly, daily intraplantar injection of NaHS enhanced, and HA prevented STZ-induced intraepidermal fiber loss, respectively. CBS was expressed in small- and medium-sized cells of DRG and co-localized with TRPV1, TRPA1 and TRPC6 in IB4-positive neurons. CONCLUSIONS: Our data suggest that H2S leads to hyperalgesia in diabetic rats through activation of TRPV1, TRPA1 and TRPC channels and, subsequent intraepidermal fibers loss. CBS enzyme inhibitors or TRP-channel blockers could be useful for treatment of painful diabetic neuropathy. SN - 1471-2202 UR - https://www.unboundmedicine.com/medline/citation/30602386/Possible_involvement_of_peripheral_TRP_channels_in_the_hydrogen_sulfide_induced_hyperalgesia_in_diabetic_rats_ L2 - https://bmcneurosci.biomedcentral.com/articles/10.1186/s12868-018-0483-3 DB - PRIME DP - Unbound Medicine ER -