| Objective:To observe the effects of different concentrations of PGE2 on the histomorphology of rabbit Achilles tendon and the expression of VEGF,b FGF and TIMP-2,and to analyze the possible mechanism of PGE2 causing Achilles tendon disease,so as to provide theoretical basis for the study of tendinopathy.Methods: Forty-eight New Zealand white rabbits were fed adaptively for one week and divided into 6 groups with 8 rabbits in each group.Group K received no intervention.Group S was injected 0.2ml of normal saline at 2.0cm of the proximal calcaneal nodule,respectively.Group A,B,C and D were injected0.2ml of 0.5ug/ml PGE2,2.5ug/ml PGE2,5ug/ml PGE2 and 10ug/ml PGE2 at the same part.One week after the end of intervention,the effects of prostaglandin E2(PGE2)on the tissue morphology of rabbit Achilles tendon and the expression of VEGF,b FGF and TIMP-2 were analyzed by comparing the differences of indicators in each group.Observation indexes :(1)The morphology and blood flow of Achilles tendon in each group were observed by ultrasound.(2)Pathological sections of Achilles tendon were made,and HE staining and Masson staining were used to observe the morphological structure of tendon tissue.(3)m RNA expression of type I and III collagen in Achilles tendon of each group was detected by PCR.(4)The expressions of VEGF,b FGF and TIMP-2 in Achilles tendon tissues of each group were detected by Western Blot.Results :(1)The ultrasonographic results showed that the tissue of rabbit Achilles tendon in group K and S was continuous and the echo was uniform.The tissue of rabbit Achilles tendon in group A and B was more continuous with A little blood flow signal and the echo was uniform.The tissue of rabbit Achilles tendon in group C and D was discontinuous with rich blood flow signal and the echo was not uniform.(2)The pathological dyeing,according to the results of collagen fiber closely packed.Group K and S order tendon cells.Group A and B of collagen fibers were slightly wavy,local collagen fiber loose,neat tendon cells,group B is also A small amount of tendon fiber fracture.Group C and D of disordered arrangement of collagen fibers,loose,irregular arrangement of tendon cell and tendon fiber breakage on the visible.(3)PCR results showed:The expression of type I collagen was determined as follows: group K(1.08±0.12),group A(1.00 ±0.07),group S(0.99±0.09),group B(0.69±0.09),group D(0.36±0.08)and group C(0.35±0.08)from high to low.Group K was compared with group S and group A showed P>0.05.Group K was compared with group B,C and D showed P<0.05.Group A was compared with group B,C and D showed P<0.05.Group B was compared with group C and D showed P<0.05.Group C was compared with group D showed P>0.05.The expression of type III collagen was determined as follows: group D(4.04 ±0.37),group C(2.97±0.28),group B(2.76±0.22),group A(1.01±0.14),group S(1.00 ±0.16)and group K(0.74±0.18).Group K was compared with group S and group A showed P>0.05.Group K was compared with group B,C and D showed P<0.05.Group B was compared with group C showed P>0.05.Group B was compared with group D showed P<0.05.Group C was compared with group D showed P<0.05.(4)Western Blot results showed:The results of VEGF expression were as follows: group C(1.61±0.01),group D(1.57±0.03),group B(1.12±0.01),group S(0.67±0.01),group A(0.66±0.02)and group K(0.56±0.02)from high to low.Group K was compared with group A,B,C,D and S showed P<0.05.Group S was compared with group B,C and D showed P<0.05.Group S was compared with group A showed P>0.05.Pairwise comparison between groups A,B,C and D showed P<0.05.The results of b FGF expression were as follows: group D(1.32±0.02),group C(1.28±0.04),group B(1.03±0.02),group A(1.03±0.01),group K(0.87±0.01)and group S(0.84±0.01)from high to low.Group K was compared with group S showed P>0.05.Group S was compared with group A,B,C and D showed P<0.05.Group A was compared with group B and C showed P>0.05. comparison between group A and group D showed P<0.05.comparison between group A and group B and C showed P>0.05.Group B was compared with group C and D showed P<0.05.Group C was compared with group D showed P>0.05.The results of TIMP-2 expression were as follows: group K(1.53±0.06),group S(1.16±0.06),group A(1.10±0.03),group B(0.80±0.03),group C(0.76±0.04),and group D(0.68±0.04).Group K was compared with group A,B,C,D and S showed P<0.05.Group S was compared with group B,C and D showed P<0.05.Group S was compared with group A showed P>0.05.Group B was compared with group C showed P>0.05.Group B was compared with group D showed P<0.05.Group C was compared with group D showed P>0.05.Conclusion:(1)Exogenous PGE2 can induce rabbit Achilles tendon tissue like tendon disease pathological changes,and the concentration dependence,namely the low concentrations of PGE2 is no obvious effect on promoting tendon disease formation,Moderate and high concentrations of PGE2 can promote the formation of tendonosis,and the concentration limit may be the 2.5ug/ml.(2)Exogenous PGE2 can increase the expression of pro-angiogenic factor(VEGF)and b FGF,decrease the expression of anti-angiogenic factor(TIMP-2),and cause local vascular hyperplasia of tendons.High concentration of PGE2 can significantly increase the vascular hyperplasia of tendons,aggravate the hypoxia and degeneration of tendons,and eventually cause tendonopathy.The concentration threshold for angiogenesis imbalance may be the 2.5ug/ml. |
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