RESUMEN
OBJECTIVE: To investigate the preventive effect of TGF-beta1 neutralizing antibody on collagen production and adhesion formation of flexor tendon. METHODS: Tendon fibroblasts, epitenon tenocytes, and endotenon tenocytes were obtained from 6 New Zealand rabbit flexor tendons. Each cell culture was supplemented with 1 ng/mL of TGF-beta along with increasing dose of TGF-beta1 neutralizing antibody. Col I production was measured by enzyme-linked immunoabsorbent assay after 3 days. Eighty-four adult New Zealand White rabbits forepaws underwent sharp transection of middle digit flexor digitorum profundus and immediate repair. Then the rabbits were divided into three groups: the normal saline (NS group, n = 36), 1.0 microg/mL TGF-beta1 neutralizing antibody (1.0 microg/mL TGF-beta1 group, n = 36) and 2.0 microg/mL TGF-beta1 neutralizing antibody (2.0 microg/mL TGF-beta1 group, n = 12) were injected in tendon sheath respectively. Tendons were harvested at 4 and 8 weeks for biomechanics testing, histological evaluation and scanning electron microscope observation. Tendons were harvested at 1, 2, 4 and 8 weeks to determine the mRNA expression of TGF-beta1 and Col I by in situ hybridization. RESULTS: ELISA exhibed that TGF-beta1 enhanced Col I production and the neutralizing antibody significantly inhibited TGF-beta1-induced Col I production in all 3 cell cultures with a dose-dependent. At 4 and 8 weeks after operation the gliding excursion of the tendon and the simulated active flexion in NS group were less than that of 1.0 microg/mL TGF-beta1 group and 2.0 microg/mL TGF-beta1 group. There was significant difference between NS group and 1.0 microg/mL TGF-beta1 group, 2.0 microg/mL TGF-beta1 group (P < 0.05). The tendon anastomosis breaking strength showed no significant differences among three groups (P > 0.05). Scanning electron microscope and histological observation showed that collagen fibers arranged irregularly in NS group, but arranged regularly in 1.0 microg/mL TGF-beta1 group and 2.0 microg/mL TGF-beta1 group at 4 and 8 weeks after operation. The in situ hybridization results revealed that TGF-beta1 and Col I mRNA expression in 1.0 microg/mL TGF-beta1 group was lower than that in NS group at each time. There was significant difference between two groups (P < 0.05). CONCLUSION: TGF-beta1 neutralizing antibody can inhibit the function of the TGF-beta1 effectively and prevent adhesion formation after the flexor tendon injured and repaired.
Asunto(s)
Anticuerpos Neutralizantes/farmacología , Colágeno/biosíntesis , Tendones/efectos de los fármacos , Tendones/metabolismo , Animales , Fenómenos Biomecánicos , Células Cultivadas , Femenino , Masculino , Conejos , Tendones/citología , Adherencias Tisulares/tratamiento farmacológico , Factor de Crecimiento Transformador beta1/inmunologíaRESUMEN
BACKGROUND: Spinal cord injury (SCI) is found to be related to increased prevalence of gallstones and acute acalculous cholecystitis. In this study we assessed the prevalence of cholelithiasis in male patients with SCI and the correlation of cholelithiasis with age and weight of patients, level of injury, as well as severity and duration of SCI. METHODS: One hundred male SCI patients (58 patients rated ASIA A or B and 42 rated ASIA C or D) aged more than 20 years (average 46.5 years) suffered from a spinal cord injury for more than one year. One hundred male volunteers served as controls without SCI and biliary diseases(age range 20-68 years; average 42.6 years). The two groups were subjected to ultrasonography of the gallbladder and biliary tract. RESULTS: The prevalence of cholelithiasis in the group of SCI patients and the control group was 26% and 10% respectively. Significant differences in the prevalence of cholelithiasis were found between the normal controls and SCI patients and between high and low-level injury (P<0.01). But the differences were not statistically significant when correlating the presence of cholelithiasis with the age and weight of the patients, the duration of SCI, and the severity of spinal lesion(P>0.05). CONCLUSIONS: SCI represents a major risk factor for the development of cholelithiasis,especially in patients with high-level injury. Cholelithiasis in SCI patients is not related to their age and weight, the severity of spinal lesion, and the duration of spinal cord injury.