Department of Biochemistry, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.
Nutrients. 2024 Jul 21;16(14):2364. doi: 10.3390/nu16142364.
Osteoarthritis (OA) is a chronic degenerative disease leading to articular cartilage destruction. Menopausal and postmenopausal women are susceptible to both OA and osteoporosis. S-equol, a soy isoflavone-derived molecule, is known to reduce osteoporosis in estrogen-deficient mice, but its role in OA remains unknown. This study aimed to explore the effect of S-equol on different degrees of menopausal OA in female Sprague-Dawley (SD) rats induced by estrogen deficiency caused by bilateral ovariectomy (OVX) combined with intra-articular injection of mono-iodoacetate (MIA). Knee joint histopathological change; serum biomarkers of bone turnover, including N-terminal propeptide of type I procollagen (PINP), C-terminal telopeptide of type I collagen (CTX-I) and N-terminal telopeptide of type I collagen (NTX-I); the cartilage degradation biomarkers hyaluronic acid (HA) and N-terminal propeptide of type II procollagen (PIINP); and the matrix-degrading enzymes matrix metalloproteinases (MMP)-1, MMP-3 and MMP-13, as well as the oxidative stress-inducing molecules nitric oxide (NO) and hydrogen peroxide (HO), were assessed for evaluation of OA progression after S-equol supplementation for 8 weeks. The results showed that OVX without or with MIA injection induced various severity levels of menopausal OA by increasing pathological damage, oxidative stress, and cartilage matrix degradation to various degrees. Moreover, S-equol supplementation could significantly reduce these increased biomarkers in different severity levels of OA. This indicates that S-equol can lessen menopausal OA progression by reducing oxidative stress and the matrix-degrading enzymes involved in cartilage degradation.
骨关节炎(OA)是一种慢性退行性疾病,导致关节软骨破坏。绝经和绝经后妇女易患 OA 和骨质疏松症。S-雌马酚,一种大豆异黄酮衍生分子,已知可减少雌激素缺乏小鼠的骨质疏松症,但它在 OA 中的作用尚不清楚。本研究旨在探讨 S-雌马酚对双侧卵巢切除(OVX)联合关节内注射单碘乙酸(MIA)诱导的雌激素缺乏绝经后 OA 不同严重程度的雌性 Sprague-Dawley(SD)大鼠的影响。膝关节组织病理学变化;骨转换的血清生物标志物,包括 I 型前胶原 N 端肽(PINP)、I 型胶原 C 端肽(CTX-I)和 I 型胶原 N 端肽(NTX-I);软骨降解生物标志物透明质酸(HA)和 II 型前胶原 N 端肽(PIINP);以及基质降解酶基质金属蛋白酶(MMP)-1、MMP-3 和 MMP-13,以及诱导氧化应激的分子一氧化氮(NO)和过氧化氢(HO),用于评估 S-雌马酚补充 8 周后 OA 进展情况。结果表明,OVX 不注射或注射 MIA 可通过增加病理损伤、氧化应激和软骨基质降解的程度,诱导不同严重程度的绝经后 OA。此外,S-雌马酚补充剂可显著降低 OA 不同严重程度的这些增加的生物标志物。这表明 S-雌马酚可以通过减少氧化应激和参与软骨降解的基质降解酶来减轻绝经后 OA 的进展。