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Volume 14, Issue 8, Pages 792-798 (September 2010)


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Effects of soy diet on inflammation-induced primary and secondary hyperalgesia in rat

Jasenka BorzanaCorresponding Author Information1email address, Jill M. Tallb1, Chengshui Zhaoc, Richard A. Meyerd, Srinivasa N. Rajaa

Received 17 August 2009; received in revised form 13 November 2009; accepted 7 December 2009. published online 11 January 2010.

Abstract 

Soy consumption is said to prevent or treat atherosclerosis, cancer, pain, and memory deficits, but experimental and clinical evidence to support these claims are lacking. We used in vivo models of inflammation to determine whether a soy diet reduces primary or secondary hyperalgesia. In all three experiments, rats were fed either a soy- or casein-based diet for at least 2weeks before induction of inflammation and for the duration of experiments. Mechanical and heat paw withdrawal thresholds and edema were measured before and several times after induction of inflammation. Primary hyperalgesia was assessed in two models: unilateral intraplantar injection with 0.1ml of 25% complete Freund’s adjuvant (CFA) or 0.1ml of 1% carrageenan. Unilateral injection of the intra-articular knee space with 25% CFA (0.1ml) was used to determine the effects of soy in a model of secondary hyperalgesia. Following intraplantar injection of CFA, soy-fed animals exhibited significantly less paw edema, mechanical allodynia, and heat hyperalgesia compared to casein-fed animals. In the carrageenan model of paw inflammation, soy-fed animals were also less allodynic to mechanical stimuli, than were casein-fed animals, but showed no diet based differences in paw edema or heat hyperalgesia. Soy diet did not affect any of the outcome measures after the intra-articular injection of CFA. Our results suggest that a soy diet significantly decreases aspects of inflammation-induced primary, but not secondary, hyperalgesia in rats.

a Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University, United States

b Department of Biological Sciences, Youngstown State University, United States

c Washington University Pain Center, Department of Anesthesiology, Washington University School of Medicine, United States

d Department of Neurosurgery, The Johns Hopkins University, Baltimore, MD, United States

Corresponding Author InformationCorresponding author. Address: The Johns Hopkins University, 720 Rutland Ave/Ross 350, Baltimore, MD 21205, United States. Tel.: +1 410 502 5510; fax: +1 410 614 2019.

 This work should be attributed to the Department of Anesthesiology and Critical Care Medicine and the Department of Neurosurgery, The Johns Hopkins University, Baltimore, MD, United States.

1 These authors equally contributed to this project.

PII: S1090-3801(09)00270-5

doi:10.1016/j.ejpain.2009.12.002


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