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Methoxsalen supplementation attenuates bone loss and inflammatory response in ovariectomized mice
Ham, Ju Ri,Choi, Ra-Yeong,Yee, Sung-Tae,Hwang, Yun-Ho,Kim, Myung-Joo,Lee, Mi-Kyung Elsevier 2017 Chemico-biological interactions Vol.278 No.-
<P><B>Abstract</B></P> <P>Methoxsalen (MTS) is a natural bioactive compound found in a variety of plants that has many known biofunctions; however, its effects on osteoporosis and related mechanisms are not clear. This study examined whether MTS exhibited preventive effects against postmenopausal osteoporosis. Female C3H/HeN mice were divided into four groups: Sham, ovariectomy (OVX), OVX with MTS (0.02% in diet), and OVX with estradiol (0.03 μg/day, s.c). After 6 weeks, MTS supplementation significantly increased femur bone mineral density and bone surface along with bone surface/total volume. MTS significantly elevated the levels of serum formation markers (estradiol, osteocalcin and bone-alkaline phosphatase) such as estradiol in OVX mice. Tartrate resistant acid phosphatase staining revealed that MTS suppressed osteoclast numbers and formation in femur tissues compared with the OVX group. Supplementation of MTS slightly up-regulated osteoblastogenesis-related genes (<I>Runx-2</I>, <I>osterix</I>, <I>osteocalcin</I>, and <I>Alp</I>) expression, whereas it significantly down-regulated inflammatory genes (<I>Nfκb</I> and <I>Il6</I>) expression in femur tissue compared with the OVX group. These results indicate that MTS supplementation effectively prevented OVX-induced osteoporosis via enhancement of bone formation and suppression of inflammatory response in OVX mice. Our study provides valid scientific information regarding the development and application of MTS as a food ingredient, a food supplement or an alternative agent for preventing postmenopausal osteoporosis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Methoxsalen improves bone mineral density in ovariectomized mice. </LI> <LI> Methoxsalen increased serum bone-ALP, osteocalcin and estradiol levels. </LI> <LI> Methoxsalen down-regulated <I>Il6</I> and <I>Nfκb</I> gene expression in femur. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Heshouwu (Polygonum multiflorum Thunb.) Extract Attenuates Bone Loss in Diabetic Mice
Ju Ri Ham,Hae-In Lee,Ra-Yeong Choi,Hyo-Seon Ryu,Sung-Tae Yee,Kyung-Yun Kang,Mi-Kyung Lee 한국식품영양과학회 2019 Preventive Nutrition and Food Science Vol.24 No.2
This study investigated the effects and mechanism of Heshouwu (Polygonum multiflorum Thunb.) water extract (HSW) on diabetes-related bone loss in mice. HSW was orally administered (300 ㎎/㎏ body weight) to high-fat diet and streptozotocin-induced diabetic mice for 10 weeks. HSW significantly alleviated mouse body weight loss and hyperglycemia compared with the control group, and elevated serum levels of insulin, osteocalcin, and bone-alkaline phosphatase. HSW supplementation also significantly increased the bone volume/tissue volume ratio and trabecular thickness and number, and decreased the bone surface/bone volume ratio and trabecular structure model index in the femur and tibia. Moreover, HSW significantly increased femoral bone mineral density. In addition, HSW down-regulated osteoclastogenic genes, such as nuclear factor of activated T-cells, cytoplasmic 1 and tartrate-resistant acid phosphatase 5 (TRAP), in both the femur and tibia tissue, and reduced serum TRAP level compare to those of control mice. These results indicate that HSW might relieve diabetes-related bone disorders through regulating osteoclast-related genes, suggesting HSW may be used as a preventive agent for diabetes-induced bone loss.
Effects of a Naphthoquinone Analog on Tumor Growth and Apoptosis Induction
Kim, Hae-Jong,Mun, Jung-Yee,Chun, Young-Jin,Choi, Kyung-Hee,Ham, Sung-Wook,Kim, Mie-Young The Pharmaceutical Society of Korea 2003 Archives of Pharmacal Research Vol.26 No.5
Vitamin K-related analogs induce growth inhibition in various cancer cell lines. A naphthoquinone analog, termed 2,3-dichloro-5, 8-dihydroxy-1,4-naphthoquinone (DDN), induces apoptosis in human promyeloid leukemic HL-60 cells, and shows antitumor activity in vivo. Following treatment with DDN, evidence of apoptosis, including DNA fragmentation and cleavage of poly ADP ribose polymerase (PARP), was observed. DDN induced an upregulation of proapoptotic Bax protein, and Bid cleavage. Antiapoptotic Bcl-2 protein levels were not changed by DDN, but the expression of Bcl-xL was decreased. In addition, DDN reduced the mass of solid tumor in the Sarcoma 180 tumor-bearing mouse model. These results indicate that DDN exerts antitumor activity, which appears to be related to the induction of apoptosis by regulating Bcl-2 family proteins.