Objective To observe any therapeutic effect of laser irradiation on pathological inflammatory reactions in ulcerative colitis (UC) induced by oxazolone,and to investigate possible mechanisms.Methods Six rats were selected as a normal control group.Another 24 rats with UC induced by oxazolone were randomly assigned to a UC model group (n =8),a 400 mW laser group (161.3 mW/cm2,n =8),and a 200 mW laser group (80.6 mW/cm2,n =8).All the rats were fixed in custom-built devices.Those in the therapy groups were treated daily,10 min per time,for 10 days.After the end of the last irradiation session,disease activity indexes (DAIs)were observed.Rats from every group were sacrificed 24 h after the last irradiation in order to observe any pathological changes in colon tissue,the weight of fresh ulcerated tissues,and gross changes in morphology.Colon segments were stained with hematoxylin-eosin and histological lesion scoring was performed under a light microscope.Any changes in inflammatory edema in the colonic mucous membrane were observed before and after laser irradiation.Results The UC model was successfully established.Average body weight in the 400 mW laser group increased significantly more than in the UC model group,approaching that of the normal control group.DAI decreased significantly.The thickness of the epithelial mucous membrane,lamina propria and submucosa was basically restored.Histological lesion scores also improved significantly,and the weight of fresh ulcerative tissue was significantly lower.Mucous membrane ulcers,submucosa edema and inflammatory cell infiltration all were alleviated significantly,merely presenting a few inflamed cells and small amounts of periphlebitis.In the 200 mW laser group all these outcome measures improved significantly compared with the UC model group,but were not as good as in the 400 mW laser group,and the rats needed longer to recover.Conclusion Laser irradiation at 400 mW has advantages over 200 mW,and could significantly relieve the pathological inflammatory response in colonic tissue,decrease submucosa edema and ameliorate other symptoms of ulcerative colitis,at least in rats.

Objective To explore the effects and molecular mechanisms of laser therapy on serum and colon tumor necrosis factor α (TNF-α),interleukin-6 (IL-6) and interleukin-10 (IL-10) in rats with oxazolone induced ulcerative colitis (UC).Methods Thirty adult male SD rats were randomly divided into four groups:a normal group ( n =6),a UC model group ( n =8 ),a 400 mW laser treatment group ( n =8 ) and a 200 mW laser treatment group ( n =8 ).Odified oxasolone sensitization was used to induce UC models in the rats.The AsAlGa semiconductor laser used in the treatment had a power of 200 mW or 400 mW.The therapy lasted for 10 days with daily 10 min sessions.The rats were sacrificed after treatment and enzyme-linked immunosorbent assay (ELISA) was used to measure IL- 6,IL- 10 and TNF-α in serum and ulcer tissues in all groups.Results Compared with the normal group,the weights of the UC model rats were significantly lower,and they had severe mucoid bloody stool.TNF-α and IL-6 levels in serum and colon tissues increased significantly and IL-10 decreased significantly,so the UC model was successfully established.After laser treatment,body weight gain and stool moderation in rats were observed.in the 400 mW group,and average TNF-α and IL-6 levels in both serum and colon tissue decreased significantly.IL-10 increased significantly,close to the level of the normal group.In the 200 mW group,serum TNF-α and IL-6 levels were significantly lower,and IL-6 in the colon tissue was reduced significantly.TNF-α did not lessen significantly,and serum and colon tissue IL-10 levels did not improve significantly compared with the model group.Conclusions 400 mW AsAlGa semiconductor laser irradiation can effectively regulate cytokines after oxaZolone induced UC in rats in two ways.It reduces pro-inflammatory cytokines and increases the level of anti-inflammatory cytokines.This may imply one of the underlying molecular mechanisms of low energy laser treatment of UC.