目的:这项研究调查了丝胶对炎症的影响,氧化应激,实验性膝骨关节炎(KOA)雌性大鼠的脂质代谢,重点通过固醇调节蛋白(SREBP)-1C和SREBP-2途径评估其有效性。
方法:将大鼠随机分为三个实验组:C组(对照组),KOA组(KOA对照),和丝胶蛋白组(KOA+丝胶)。通过将碘乙酸钠(MIA)注射到膝关节中创建KOA模型。在第1、7、14和21天对大鼠关节内施用丝胶(0.8g/kg/mL,50微升)。21天后,老鼠被处死,和血清样品分析使用ELISA测量肿瘤坏死因子-α(TNF-α),白细胞介素-1β(IL-1β),IL-10,SREBP-1c,SREBP-2,乙酰辅酶A羧化酶(ACC),脂肪酸合成酶(FAS),胆固醇,甘油三酯,和总氧化剂-抗氧化剂状态(TOS-TAS)水平。
结果:KOA组血清TNF-α升高,IL-1β,TOS,SREBP-1C,ACC,FAS,甘油三酯,SREBP-2、胆固醇程度优于C组(P<0.05)。然而,这些细胞因子的水平,除了胆固醇,丝胶蛋白组明显低于KOA组。KOA组血清TAS和IL-10水平明显低于C组(P<0.05)。在丝胶组中,增加有统计学意义(P<0.05)。
结论:丝胶显示出减少炎症的潜力,氧化应激,大鼠KOA实验模型中的脂质代谢。然而,需要进一步的临床研究来验证丝胶作为KOA治疗药物的潜力.要点•丝胶可以减轻实验性大鼠模型中的膝骨关节炎(KOA)症状。•Inparticular,在实验性KOA大鼠模型的血清中,丝胶特别降低促炎细胞因子的水平,如肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β),并增加抗炎细胞因子的水平,例如IL-10。•丝胶通过甾醇调节蛋白(SREBP)-1C和SREBP-2途径和实验性KOA大鼠模型的血清中的氧化应激降低脂质代谢。•丝胶的关节内给药已被证明可显着降低脂质代谢,氧化应激,和炎症,在生化分析的支持下。这些发现表明其作为KOA替代治疗方案的潜力巨大。
OBJECTIVE: This study investigated the effects of
sericin on inflammation, oxidative stress, and lipid metabolism in female rats with experimental knee osteoarthritis (KOA), focusing on evaluating its effectiveness via the sterol regulatory protein (SREBP)-1C and SREBP-2 pathways.
METHODS: The rats were randomly assigned to three experimental groups: the C group (control), the KOA group (KOA control), and the sericin group (KOA +
sericin). The KOA model was created by injecting monosodium iodoacetate (MIA) into the knee joint.
Sericin was administered intra-articularly to rats on days 1, 7, 14, and 21 (0.8 g/kg/mL, 50 µL). After 21 days, the rats were sacrificed, and serum samples were analyzed using an ELISA to measure tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-10, SREBP-1c, SREBP-2, acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), cholesterol, triglyceride, and total oxidant-antioxidant status (TOS-TAS) levels.
RESULTS: The KOA group exhibited higher serum TNF-α, IL-1β, TOS, SREBP-1C, ACC, FAS, triglyceride, SREBP-2, and cholesterol levels than the C group (P < 0.05). However, the levels of these cytokines, except cholesterol, were significantly lower in the sericin group than in the KOA group. The KOA group exhibited significantly lower serum TAS and IL-10 levels than the C group (P < 0.05). In the
sericin group, there was a statistically significant increase (P < 0.05).
CONCLUSIONS: Sericin shows promising potential for reducing inflammation, oxidative stress, and lipid metabolism in experimental models of KOA in rats. However, further clinical research is necessary to validate the potential of sericin as a therapeutic agent for treating KOA. Key Points • Sericin can reduce knee osteoarthritis (KOA) symptoms in an experimental rat model. • In particular, in the serum of an experimental KOA rat model, sericin specifically reduces the levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β), and increases the levels of anti-inflammatory cytokines, such as IL-10. • Sericin reduced lipid metabolism via the sterol regulatory protein (SREBP)-1C and SREBP-2 pathways and oxidative stress in the serum of the experimental KOA rat model. • The intra-articular administration of sericin has been shown to significantly reduce lipid metabolism, oxidative stress, and inflammation, as supported by biochemical analysis. These findings suggest its promising potential as an alternative treatment option for KOA.