Effects of Jaoga-Yukmiwon®, a Korean herbal medicine, on chondrocyte proliferation and longitudinal bone growth in adolescent male rats

2003 ◽  
Vol 17 (9) ◽  
pp. 1113-1116 ◽  
Author(s):  
K. Leem ◽  
S. Y. Park ◽  
D. H. Lee ◽  
Y. M. Boo ◽  
K. H. Cho ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Bone Growth ◽  
Male Rats ◽  
Adolescent Male ◽  
Chondrocyte Proliferation ◽  
Longitudinal Bone Growth

scholarly journals Effects of Laser Acupuncture on Longitudinal Bone Growth in Adolescent Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Mijung Yeom ◽  
Sung-Hun Kim ◽  
Bina Lee ◽  
Xiuyu Zhang ◽  
Hyangsook Lee ◽  
...  
Keyword(s):  
Growth Rate ◽  
Growth Plate ◽  
Bone Growth ◽  
Growth Potential ◽  
Male Rats ◽  
Adolescent Male ◽  
Laser Acupuncture ◽  
Longitudinal Bone Growth ◽  
Level Laser ◽  
Adolescent Rats

Longitudinal bone growth is the results of chondrocyte proliferation and hypertrophy and subsequent endochondral ossification in the growth plate. Recently, laser acupuncture (LA), an intervention to stimulate acupoint with low-level laser irradiation, has been suggested as an intervention to improve the longitudinal bone growth. This study investigated the effects of laser acupuncture on growth, particularly longitudinal bone growth in adolescent male rats. Laser acupuncture was performed once every other day for a total of 9 treatments over 18 days to adolescent male rats. Morphometry of the growth plate, longitudinal bone growth rate, and the protein expression of BMP-2 and IGF-1 in growth plate were observed. The bone growth rate and the heights of growth plates were significantly increased by laser acupuncture. BMP-2 but not IGF-1 immunostaining in growth plate was increased as well. In conclusion, LA promotes longitudinal bone growth in adolescent rats, suggesting that laser acupuncture may be a promising intervention for improving the growth potential for children and adolescents.

scholarly journals Effects of Egg Yolk Proteins on the Longitudinal Bone Growth of Adolescent Male Rats

2004 ◽  
Vol 68 (11) ◽  
pp. 2388-2390 ◽  
Author(s):  
Kang-Hyun LEEM ◽  
Myung-Gyou KIM ◽  
Hyun-Mi KIM ◽  
Mujo KIM ◽  
Young-Ja LEE ◽  
...  
Keyword(s):  
Bone Growth ◽  
Egg Yolk ◽  
Male Rats ◽  
Adolescent Male ◽  
Yolk Proteins ◽  
Longitudinal Bone Growth

Sites of action of testosterone and estradiol on longitudinal bone growth

1983 ◽  
Vol 244 (2) ◽  
pp. E135-E140 ◽  
Author(s):  
J. O. Jansson ◽  
S. Eden ◽  
O. Isaksson
Keyword(s):  
Replacement Therapy ◽  
Bone Growth ◽  
Body Weight Gain ◽  
Inhibitory Effect ◽  
Body Growth ◽  
Female Rats ◽  
Male Rats ◽  
Longitudinal Bone Growth ◽  
Sites Of Action ◽  
Different Doses

In this study the mechanisms by which sex steroids influence body growth were investigated. The effect of different doses of testosterone propionate on longitudinal bone growth and body weight gain was studied in a) gonadectomized male rats, b) gonadohypophysectomized male rats, and c) gonadohypophysectomized male rats given replacement therapy with bovine growth hormone (bGH). The effect of different doses of estradiol benzoate on the same growth parameters was studied in female rats divided into the same experimental groups as the males. Accumulated longitudinal bone growth was determined using oxytetracycline as an intravital marker. Testosterone caused a dose-dependent increase in longitudinal bone growth in gonadectomized male rats. In contrast, testosterone exerted no significant increase in longitudinal bone growth in gonadohypophysectomized male rats with and without bGH replacement therapy. Treatment with estrogen inhibited longitudinal bone growth and body weight gain. The inhibitory effect of estradiol was approximately the same in gonadohypophysectomized female rats given bGH replacement therapy as in gonadectomized female rats. The results suggest that testosterone exerts its stimulatory effect on body growth mainly by modulating hypothalamopituitary functions, e.g., by altering the secretory pattern of GH. On the other hand, it seems that changes in the hypothalamopituitary functions are less significant for the inhibitory effect of estradiol on body growth. It is concluded from this study that the sites of action for estrogen and testosterone in modulating body growth in the rat are different.

scholarly journals Nuclear Factor-κB p65 Facilitates Longitudinal Bone Growth by Inducing Growth Plate Chondrocyte Proliferation and Differentiation and by Preventing Apoptosis

2007 ◽  
Vol 282 (46) ◽  
pp. 33698-33706 ◽  
Author(s):  
Shufang Wu ◽  
Janna K. Flint ◽  
Geoffrey Rezvani ◽  
Francesco De Luca
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Chondrocyte Apoptosis ◽  
Pyrrolidine Dithiocarbamate ◽  
Growth Plate Chondrocytes ◽  
Chondrocyte Proliferation ◽  
Longitudinal Bone Growth ◽  
Metatarsal Bones ◽  
Proliferation And Differentiation ◽  
Cultured Chondrocytes

NF-κB is a group of transcription factors involved in cell proliferation, differentiation, and apoptosis. Mice deficient in the NF-κB subunits p50 and p52 have retarded growth, suggesting that NF-κB is involved in bone growth. Yet, it is not clear whether the reduced bone growth of these mice depends on the lack of NF-κB activity in growth plate chondrocytes. Using cultured rat metatarsal bones and isolated growth plate chondrocytes, we studied the effects of two NF-κB inhibitors (pyrrolidine dithiocarbamate (PDTC) or BAY11-7082 (BAY)), p65 short interference RNA (siRNA), and of the overexpression of p65 on chondrocyte proliferation, differentiation, and apoptosis. To further define the underlying mechanisms, we studied the functional interaction between NF-κB p65 and BMP-2 in chondrocytes. PDTC and BAY suppressed metatarsal linear growth. Such growth inhibition resulted from decreased chondrocyte proliferation and differentiation and from increased chondrocyte apoptosis. In cultured chondrocytes, the inhibition of NF-κB p65 activation (by PDTC and BAY) and expression (by p65 siRNA) led to the same findings observed in cultured metatarsal bones. In contrast, overexpression of p65 in cultured chondrocytes induced chondrocyte proliferation and differentiation and prevented apoptosis. Although PDTC, BAY, and p65 siRNA reduced the expression of BMP-2 in cultured growth plate chondrocytes, the overexpression of p65 increased it. The addition of Noggin, a BMP-2 antagonist, neutralized the stimulatory effects of p65 on chondrocyte proliferation and differentiation, as well as its anti-apoptotic effect. In conclusion, our findings indicate that NF-κB p65 expressed in growth plate chondrocytes facilitates growth plate chondrogenesis and longitudinal bone growth by inducing BMP-2 expression and activity.

scholarly journals DHEA Suppresses Longitudinal Bone Growth by Acting Directly at Growth Plate through Estrogen Receptors

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1423-1433 ◽  
Author(s):  
Hongzhi Sun ◽  
Weijin Zang ◽  
Bo Zhou ◽  
Lin Xu ◽  
Shufang Wu
Keyword(s):  
Estrogen Receptor ◽  
Growth Plate ◽  
Bone Growth ◽  
Nuclear Factor Κb ◽  
Binding Activity ◽  
Skeletal Maturation ◽  
Chondrocyte Apoptosis ◽  
Chondrocyte Proliferation ◽  
Longitudinal Bone Growth ◽  
Growth Plate Chondrocyte

Abstract Dehydroepiandrosterone (DHEA) is produced by the adrenal cortex and is the most abundant steroid in humans. Although in some physiological and pathological conditions the increased secretion of DHEA and its sulfated form is associated with accelerated growth rate and skeletal maturation, it is unclear whether DHEA can affect longitudinal bone growth and skeletal maturation by acting directly at the growth plate. In our study, DHEA suppressed metatarsal growth, growth plate chondrocyte proliferation, and hypertrophy/differentiation. In addition, DHEA increased the number of apoptotic chondrocytes in the growth plate. In cultured chondrocytes, DHEA reduced chondrocyte proliferation and induced apoptosis. The DHEA-induced inhibition of metatarsal growth and growth plate chondrocyte proliferation and hypertrophy/differentiation was nullified by culturing metatarsals with DHEA in the presence of ICI 182,780, an inhibitor of estrogen receptor, but not in the presence of Casodex, an inhibitor of androgen receptor. Lastly, nuclear factor-κB DNA binding activity was inhibited by the addition of DHEA in the medium of cultured chondrocyte. Our findings indicate that DHEA suppressed bone growth by acting directly at growth plate through estrogen receptor. Such growth inhibition is mediated by decreased chondrocyte proliferation and hypertrophy/differentiation and by increased chondrocyte apoptosis.

scholarly journals The role of estrogen receptor-α and its activation function-1 for growth plate closure in female mice

2012 ◽  
Vol 302 (11) ◽  
pp. E1381-E1389 ◽  
Author(s):  
A. E. Börjesson ◽  
S. H. Windahl ◽  
E. Karimian ◽  
E. E. Eriksson ◽  
M. K. Lagerquist ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Growth Plate ◽  
Bone Growth ◽  
High Dose ◽  
Plate Height ◽  
Chondrocyte Proliferation ◽  
Growth Plates ◽  
Longitudinal Bone Growth ◽  
Female Mice

High estradiol levels in late puberty induce growth plate closure and thereby cessation of growth in humans. In mice, the growth plates do not fuse after sexual maturation, but old mice display reduced longitudinal bone growth and high-dose estradiol treatment induces growth plate closure. Estrogen receptor (ER)-α stimulates gene transcription via two activation functions (AFs), AF-1 and AF-2. To evaluate the role of ERα and its AF-1 for age-dependent reduction in longitudinal bone growth and growth plate closure, female mice with inactivation of ERα (ERα−/−) or ERαAF-1 (ERαAF-10) were evaluated. Old (16- to 19-mo-old) female ERα−/− mice showed continued substantial longitudinal bone growth, resulting in longer bones (tibia: +8.3%, P < 0.01) associated with increased growth plate height (+18%, P < 0.05) compared with wild-type (WT) mice. In contrast, the longitudinal bone growth ceased in old ERαAF-10 mice (tibia: −4.9%, P < 0.01). Importantly, the proximal tibial growth plates were closed in all old ERαAF-10 mice while they were open in all WT mice. Growth plate closure was associated with a significantly altered balance between chondrocyte proliferation and apoptosis in the growth plate. In conclusion, old female ERα−/− mice display a prolonged and enhanced longitudinal bone growth associated with increased growth plate height, resembling the growth phenotype of patients with inactivating mutations in ERα or aromatase. In contrast, ERαAF-1 deletion results in a hyperactive ERα, altering the chondrocyte proliferation/apoptosis balance, leading to growth plate closure. This suggests that growth plate closure is induced by functions of ERα that do not require AF-1 and that ERαAF-1 opposes growth plate closure.

Peripubertal Caffeine Exposure Impairs Longitudinal Bone Growth in Immature Male Rats in a Dose- and Time-Dependent Manner

2016 ◽  
Vol 19 (1) ◽  
pp. 73-84 ◽  
Author(s):  
Yun-Young Choi ◽  
Yuri Choi ◽  
Jisook Kim ◽  
Hyeonhae Choi ◽  
Jiwon Shin ◽  
...  
Keyword(s):  
Bone Growth ◽  
Time Dependent ◽  
Male Rats ◽  
Dependent Manner ◽  
Longitudinal Bone Growth ◽  
Immature Male ◽  
Caffeine Exposure

Antarctic krill oil promotes longitudinal bone growth in adolescent male mice

2019 ◽  
Vol 28 ◽  
pp. 170-176 ◽  
Author(s):  
Qiping Zhan ◽  
Yingying Tian ◽  
Yufeng Dai ◽  
Yanqi Li ◽  
Yuanyuan Li ◽  
...  
Keyword(s):  
Bone Growth ◽  
Antarctic Krill ◽  
Adolescent Male ◽  
Krill Oil ◽  
Male Mice ◽  
Longitudinal Bone Growth ◽  
Antarctic Krill Oil
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