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Elevated H2 O2 levels in trinitrobenzene sulfate-induced colitis rats contributes to visceral hyperalgesia through interaction with the transient receptor potential ankyrin 1 cation channel.
J Gastroenterol Hepatol 2016; 31(6):1147-53JG

Abstract

BACKGROUND AND AIM

Inflammatory bowel disease is associated with chronic abdominal pain. Transient receptor potential ankyrin 1 (TRPA1) is a well-known pain sensor expressed in primary sensory neurons. Recent studies indicate that reactive oxygen species such as hydrogen peroxide (H2 O2) may activate TRPA1.

METHODS

Colonic inflammation was induced by intra-colonic administration of trinitrobenzene sulfate (TNBS) in adult male Sprague-Dawley rats. Visceromotor response (VMR) to colorectal distention (CRD) was recorded to evaluate the visceral hyperalgesia. Rats were sacrificed 1 day after treatment with saline or TNBS; colonic tissues from the inflamed region were removed and then processed to assess the H2 O2 content. H2 O2 scavenger N-acetyl-l-cysteine or a TRPA1 antagonist, HC-030031, was intravenously administrated to the TNBS-treated rats or saline-treated rats. In a parallel experiment, intra-colonic H2 O2 -induced visceral hyperalgesia in naïve rats and the effect of intravenous HC-030031 were measured based on the VMR to CRD.

RESULTS

Trinitrobenzene sulfate treatment resulted in significant increase in VMR to CRD at day 1. The H2 O2 content in the inflamed region of the colon in TNBS-treated rats was significantly higher than that of saline-treated rats. N-acetyl-l-cysteine or HC-030031 significantly suppressed the enhanced VMR in TNBS-treated rats while saline-treated rats remained unaffected. Moreover, blockade of TRPA1 activation by HC-030031 significantly reversed the exogenous H2 O2 -induced visceral hyperalgesia.

CONCLUSION

These results suggest that H2 O2 content of the colonic tissue is increased in the early stage of TNBS-induced colitis. The increased H2 O2 content may contribute to the visceral hyperalgesia by activating TRPA1.

Authors+Show Affiliations

Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan.Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan. Traditional Medicine Research Center, Chinese Medicine Confucius Institute, Hyogo College of Medicine, Kobe, Hyogo, 6508530, Japan.Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan.Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan.Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan.Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan.Traditional Medicine Research Center, Chinese Medicine Confucius Institute, Hyogo College of Medicine, Kobe, Hyogo, 6508530, Japan. Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo, 6508530, Japan. Traditional Medicine Research Center, Chinese Medicine Confucius Institute, Hyogo College of Medicine, Kobe, Hyogo, 6508530, Japan. Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26574143

Citation

Kogure, Yoko, et al. "Elevated H2 O2 Levels in Trinitrobenzene Sulfate-induced Colitis Rats Contributes to Visceral Hyperalgesia Through Interaction With the Transient Receptor Potential Ankyrin 1 Cation Channel." Journal of Gastroenterology and Hepatology, vol. 31, no. 6, 2016, pp. 1147-53.
Kogure Y, Wang S, Tanaka K, et al. Elevated H2 O2 levels in trinitrobenzene sulfate-induced colitis rats contributes to visceral hyperalgesia through interaction with the transient receptor potential ankyrin 1 cation channel. J Gastroenterol Hepatol. 2016;31(6):1147-53.
Kogure, Y., Wang, S., Tanaka, K., Hao, Y., Yamamoto, S., Nishiyama, N., ... Dai, Y. (2016). Elevated H2 O2 levels in trinitrobenzene sulfate-induced colitis rats contributes to visceral hyperalgesia through interaction with the transient receptor potential ankyrin 1 cation channel. Journal of Gastroenterology and Hepatology, 31(6), pp. 1147-53. doi:10.1111/jgh.13226.
Kogure Y, et al. Elevated H2 O2 Levels in Trinitrobenzene Sulfate-induced Colitis Rats Contributes to Visceral Hyperalgesia Through Interaction With the Transient Receptor Potential Ankyrin 1 Cation Channel. J Gastroenterol Hepatol. 2016;31(6):1147-53. PubMed PMID: 26574143.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Elevated H2 O2 levels in trinitrobenzene sulfate-induced colitis rats contributes to visceral hyperalgesia through interaction with the transient receptor potential ankyrin 1 cation channel. AU - Kogure,Yoko, AU - Wang,Shenglan, AU - Tanaka,Koh-Ichi, AU - Hao,Yongbiao, AU - Yamamoto,Satoshi, AU - Nishiyama,Nobuyoshi, AU - Noguchi,Koichi, AU - Dai,Yi, PY - 2015/07/30/received PY - 2015/10/14/revised PY - 2015/11/04/accepted PY - 2015/11/18/entrez PY - 2015/11/18/pubmed PY - 2017/5/17/medline KW - H2O2 KW - IBD KW - TNBS KW - TRPA1 KW - visceral pain SP - 1147 EP - 53 JF - Journal of gastroenterology and hepatology JO - J. Gastroenterol. Hepatol. VL - 31 IS - 6 N2 - BACKGROUND AND AIM: Inflammatory bowel disease is associated with chronic abdominal pain. Transient receptor potential ankyrin 1 (TRPA1) is a well-known pain sensor expressed in primary sensory neurons. Recent studies indicate that reactive oxygen species such as hydrogen peroxide (H2 O2) may activate TRPA1. METHODS: Colonic inflammation was induced by intra-colonic administration of trinitrobenzene sulfate (TNBS) in adult male Sprague-Dawley rats. Visceromotor response (VMR) to colorectal distention (CRD) was recorded to evaluate the visceral hyperalgesia. Rats were sacrificed 1 day after treatment with saline or TNBS; colonic tissues from the inflamed region were removed and then processed to assess the H2 O2 content. H2 O2 scavenger N-acetyl-l-cysteine or a TRPA1 antagonist, HC-030031, was intravenously administrated to the TNBS-treated rats or saline-treated rats. In a parallel experiment, intra-colonic H2 O2 -induced visceral hyperalgesia in naïve rats and the effect of intravenous HC-030031 were measured based on the VMR to CRD. RESULTS: Trinitrobenzene sulfate treatment resulted in significant increase in VMR to CRD at day 1. The H2 O2 content in the inflamed region of the colon in TNBS-treated rats was significantly higher than that of saline-treated rats. N-acetyl-l-cysteine or HC-030031 significantly suppressed the enhanced VMR in TNBS-treated rats while saline-treated rats remained unaffected. Moreover, blockade of TRPA1 activation by HC-030031 significantly reversed the exogenous H2 O2 -induced visceral hyperalgesia. CONCLUSION: These results suggest that H2 O2 content of the colonic tissue is increased in the early stage of TNBS-induced colitis. The increased H2 O2 content may contribute to the visceral hyperalgesia by activating TRPA1. SN - 1440-1746 UR - https://www.unboundmedicine.com/medline/citation/26574143/Elevated_H2_O2_levels_in_trinitrobenzene_sulfate_induced_colitis_rats_contributes_to_visceral_hyperalgesia_through_interaction_with_the_transient_receptor_potential_ankyrin_1_cation_channel_ L2 - https://doi.org/10.1111/jgh.13226 DB - PRIME DP - Unbound Medicine ER -