Pirfenidone improves scar contracture of the knee joint after seawater immersion in rabbits
ZHANG Yongguang1, SHENG Qingsong2, QIU Zhuo3, HU Jianwei1, CHEN Jianmei1, YE Yongping1
1. Department of Orthopedics, 2. Department of Obstetrics-Gynecology, 3. Comprehensive Planning Office, 900th Hospital of the Joint Logistics Support Force, Fuzhou 350025, China
Abstract:Objective To investigate the effect of oral administration of Pirfenidone (PFN) on scar contracture of the knee joint after seawater immersion.Methods According to the random-number-table method, 20 rabbits were randomly divided into four groups (n=5): normal saline control group (NS group), seawater control group (SW group), normal saline+PFN treatment group (NS+PFN group), and seawater+PFN treatment group (SW+PFN group). Animals in the PFN treatment groups were given 0.75 g of PFN daily (within normal feedstuffs), while animals in the control groups were given normal feedstuffs only. After 4 weeks, the animals were killed, and the suprapatellar bursa was collected for Masson staining. The content of hydroxyproline and TGF-β1 were detected by ELISA. Results The incision healed well. After Pirfenidone treatment, Masson staining results showed that collagen fibers of incision scar were relatively sparse, roughly parallel arrangement, and the performance was relatively regular. The results showed that the levels of hydroxyproline were (114.20±14.54) ng/ml, (99.21±18.27) ng/ml, (87.91±12.02) ng/ml and (76.17±18.72) ng/ml in SW group, NS group, SW+PFN group and NS+PFN group, respectively. The level of hydroxyproline in SW+PFN group was significantly lower than that in SW group (P<0.05). Further detection showed that the levels of TGF-β1 in SW group and SW+PFN group were (151.53±20.21) ng/ml and (106.53±12.86) ng/ml, respectively. The level of TGF-β1 in SW+PFN group was significantly lower than that in SW group (P<0.05). Conclusions Pirfenidone can alleviate the scar contracture around the knee joint after seawater immersion and improve the joint dysfunction. The mechanism underlying may be related to the inhibition of collagen synthesis and the down-regulation of TGF-β1 level.
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