Objective To observe the effect of Melittin on collagen type II (Col-II) expression of rat endplate chondrocytes (EPCs) induced by interleukin 1β (IL-1β). Methods Primary EPCs from the lumbar vertebra of 4-week-old Sprague Dawley rats were culturedin vitro and identified by morphological observation, toluidine blue staining and Col-II immunofluorescence staining. Then, MTT assay was used to determine the optimal concentration of IL-1 and Melittin. Next, EPCs at passage 3 were randomly divided into 4 groups: no treatment was done in group A as control group; the optimal concentration of IL-1β, Melittin, and both IL-1β and Melittin were used in groups B, C, and D respectively. The expression of Col-II was detected by Western blot after 48 hours intervention. Results Under inverted microscope, the first generation EPCs were polygonal; cell proliferation decreased after fifth generation, and cell morphology changed into fusiform. The acidic mucosubstance in the cytoplasm (such as Aggrecan) was stained dark blue by toluidine blue. After marking Col-II by immunofluorescence, the positive expression of cytoskeleton (green fluorescence) could be observed. MTT assay showed that IL-1β and Melittin could inhibit the EPCs in a dose-dependent manner after intervention of 24 and 48 hours, and the optimal concentrations of IL-1β and Melittin intervention were 10 ng/mL and 1.0 μg/mL respectively. Compared with group A, the expression of Col-II was significantly reduced in group B, and was significantly increased in group C by Western blot assay, but there was no significant difference between group D and group A. The Col-II expression levels of groups A, B, C, and D were 0.991±0.024, 0.474±0.127, 1.913±0.350, and 1.159±0.297 respectively, showing significant difference between the other groups (P<0.05) except between group A and group D (P>0.05). Conclusion Melittin has a protective effect on endplate cartilage, and the research results provide experimental basis for the prevention and treatment of spinal degenerative disease.
Objective To investigate the effectiveness of the free fibular skin flap of the great toe in repairing finger flexion deformity due to scar contracture. Methods The clinical data of 12 patients with finger flexion deformity due to scar contracture treated with scar release and free fibular skin flap of the great toe between March 2022 and December 2024 was retrospectively analyzed. All patients had flexion deformity caused by scar contracture of finger joints after healing of skin defect scar. The duration of scar contracture ranged from 3 months to 2 years, with an average of 7 months. The active range of motion of the finger joint was 0°-10°, with an average of 8°. The range of skin flap was 2.0 cm×1.3 cm to 3.5 cm×2.5 cm. Results All 12 patients were followed up 6-12 months, with an average of 10.5 months. At last follow-up, the flexion deformity of the affected finger was completely corrected, and the active range of motion of the finger joint was restored to close to the healthy side (the distal finger joint was 30°-40°, with an average of 35°; the proximal finger joint was 80°-90°, with an average of 85°). The shape of the flap was plump, the texture was good, and the static two-point discrimination was 6-8 mm, with an average of 6.8 mm. According to the evaluation standard of upper limb function of Chinese Medical Association Hand Surgery Society, 9 cases were excellent, 3 cases were good, and the excellent and good rate was 100%. All wounds at donor sites healed by first intention, with no pain, ulcer or ulceration in toes, normal walking in shoes, and no influence on gait. Conclusion Free fibular skin flap of the great toe is an effective method to repair the finger flexion deformity due to scar contracture, which providing good cosmetic, motor, and sensory outcomes with low donor-site morbidity.