TNF-α Will Express In Rat Achilles Tendon Lesion In The End Zone Under Stress Stimulation

Purposes：There has been a great number of studies on TNF-αand TNF-κB’s signalingpathways and the relationship between these two. However, the study of their effects onthe incidence of Enthesiopathy is still on the exploratory stage, with few direct studies.As an important inflammatory cytokine, TNF-α alone, or by interaction with othercytokines, enhances the inflammation. NF-κB signaling pathway is involved in theformation of Enthesiopathy in many ways. But, since this is a complex cell cytokinenetwork, the specific regulatory and feedback regulatory mechanisms, the interaction ofcytokine network and the possible link between signaling pathways remain to begradually revealed. Thus, further studies on TNF-α-mediated NF-κB signaling pathways,especially the study on TNF-α and NF-κB inhibitors treatment for enthesiopathy, mayprovide a new attempt to delay or block the enthesiopathy process, and provide atheoretical basis for early prevention and clinical treatment for enthesiopathy.Methods：308-week-old male SD rats purchased from the Experimental Animal Center ofSoochow University were randomly separated as control groups (6) and experimentalgroup (24). The rats in the control groups will be regularly feed under normalcircumstances, while the experimental group is put in the cage with semi-automaticjumping electrical stimulation for a period of six-week jumping movement. For onceevery two weeks, rats were killed to get their achilles tendon and proximal heel bonearea of their hind feet. A group of materials will be used to assay the tissue TNF-α andNF-κB protein content through immunohistochemical method and the other will bemade into HE paraffin sections for staining and observation. With comparison of thehistopathological changes in the Achilles tendon terminal region for the3experimental groups and the control groups, analyze the expression of TNF-α and NF-κB indifferent groups.Results：(1)HE staining shows that there are great differences in pathological tissuemorphologies between the experimental groups and the control groups, differenceincreased significantly with the extension of modeling time.(2)For the control group of rats after2,4and6weeks, there are no significantdifferences (p>0.05) in the number of TNF-α-positive cells in their tendon, fibrous,calcified cartilage and calcaneus. While for the experimental groups after2,4,6weeksof jumping, the number of TNF-α-positive cells increase significantly in their tendon,fibrous, calcified cartilage and calcaneus, with significant difference (P <0.01).(3)For the control group of rats after2,4and6weeks, there are no significantdifferences (p>0.05) in the number of NF-κB-positive cells in their tendon, fibrous,calcified cartilage and calcaneus. While for the experimental groups after2,4,6weeks ofjumping, the number of NF-κB-positive cells increase significantly in their tendon,fibrous, calcified cartilage and calcaneus, with significant difference (P <0.01).Conclusion：(1)The phenomena that TNF-α and NF-κB become sensitive to stress stimuli, and TNF-α and NF-κB expression increase, are one of the mechanisms that enthesiopathy generated.(2) Different district of the end zone consists of different levels of TNF-α and NF-κB, with higher levels in fiber and calcification of tendons and cartilage area, whilelower levels in bone area.