Department of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Hanpoong Pharm and Foods Co., Ltd., Jeonju 561-841, Republic of Korea.
J Microbiol Biotechnol. 2020 Oct 28;30(10):1543-1551. doi: 10.4014/jmb.2004.04016.
has a wide range of activities including a neuroprotective effect, skin protective effects, enhanced DNA repairing, anti-diabetic activity, and protective effects against vascular inflammation. In the present study, we sought to discover the inhibitory effects of a mixture of natural products containing and (PZRAS) on osteoclastogenesis and bone remodeling, as neither the effects of a mixture containing , nor its molecular mechanism on bone inflammation, have been clarified yet. PZRAS upregulated the levels of catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GSH-R) and glutathione peroxidase (GSH-Px) and reduced malondialdehyde (MDA) in LPS-treated RAW264.7 cells. Moreover, treatment with PZRAS decreased the production of IL-1β and TNF-α. PZRAS also inhibited osteoclast differentiation through inhibiting osteoclastspecific genes like MMP-2, 9, cathepsin K, and TRAP in RANKL-treated RAW264.7 cells. Additionally, PZRAS has inhibitory functions on the RANKL-stimulated activation of ERK and JNK, which lead to a decrease in the expression of NFATc1 and c-Fos. In an in vivo study, bone resorption induced by LPS was recovered by treatment with PZRAS in bone volume per tissue volume (BV/TV) compared to control. Furthermore, the ratio of eroded bone surface of femurs was significantly increased in LPStreated mice compared to vehicle group, but this ratio was significantly reversed in PZRAS-treated mice. These results suggest that PZRAS could prevent or treat disorders with abnormal bone loss.
具有广泛的活性，包括神经保护作用、皮肤保护作用、增强 DNA 修复、抗糖尿病活性和血管炎症保护作用。在本研究中，我们试图发现包含 和 （PZRAS）的天然产物混合物对破骨细胞生成和骨重塑的抑制作用，因为目前尚未阐明包含 混合物的作用及其对骨炎症的分子机制。PZRAS 上调了 LPS 处理的 RAW264.7 细胞中过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、谷胱甘肽还原酶 (GSH-R) 和谷胱甘肽过氧化物酶 (GSH-Px) 的水平，并降低了丙二醛 (MDA) 的水平。此外，PZRAS 处理还降低了 IL-1β 和 TNF-α 的产生。PZRAS 还通过抑制 RANKL 处理的 RAW264.7 细胞中 MMP-2、9、组织蛋白酶 K 和 TRAP 等破骨细胞特异性基因的表达来抑制破骨细胞分化。此外，PZRAS 对 RANKL 刺激的 ERK 和 JNK 激活具有抑制作用，导致 NFATc1 和 c-Fos 的表达减少。在体内研究中，与对照组相比，PZRAS 处理可使 LPS 诱导的骨吸收在组织体积骨体积比（BV/TV）中恢复。此外，与 vehicle 组相比，LPS 处理的小鼠股骨侵蚀骨表面的比例显著增加，但在 PZRAS 处理的小鼠中，该比例显著逆转。这些结果表明，PZRAS 可预防或治疗异常骨丢失的疾病。
