I wrote about Resveratrol before and it is available for sale.
“Osteoporosis is a major public health issue that is expected to rise as the global population ages. Resveratrol (RES) is a plant polyphenol with various anti-aging properties. RES treatment of bone cells results in protective effects, but dose translation from in vitro studies to clinically relevant doses is limited since bioavailability is not taken into account. The aims of this review is to evaluate in vivo evidence for a role of RES supplementation in promoting bone health to reduced osteoporosis risk and potential mechanisms of action. Due to multiple actions on both osteoblasts and osteoclasts, RES has potential to attenuate bone loss resulting from different etiologies and pathologies. Several animal models have investigated the bone protective effects of RES supplementation. Ovariectomized rodent models of rapid bone loss due to estrogen-deficiency reported that RES supplementation improved bone mass and trabecular bone without stimulating other estrogen-sensitive tissues. RES supplementation prior to age-related bone loss was beneficial. The hindlimb unloaded rat model used to investigate bone loss due to mechanical unloading showed RES supplementation attenuated bone loss in old rats, but had inconsistent bone effects in mature rats. In growing rodents, RES increased longitudinal bone growth, but had no other effects on bone. In the absence of human clinical trials, evidence for a role of RES on bone heath relies on evidence generated by animal studies.”
“Resveratrol (RES) is a polyphenolic (3,4’,5-trihydroxystilbene) compound naturally present in red wine and a variety of plant foods such as grapes, cranberries, and nuts”
” human bone marrow-derived MSC with RES increased gene expression of the key osteogenic transcription factors, Runx2 and Osterix. RES was also demonstrated in vitro to act on various signal transduction pathways. RES activated the estrogen-mediated extracellular signal-regulated kinase 1/2 (ERK) signaling pathway regulating osteoblast differentiation and proliferation. RES activated AMP-activated protein kinase (AMPK) which regulates osteoblast differentiation and inhibits bone resorption by acting as a negative regulator of RANKL. RES augmented Wnt signaling which stimulated osteoblastogenesis and bone formation. Treating human bone marrow-derived MSC with RES promoted differentiation of MSC towards osteoblasts by up-regulating Runx2 gene expression through the activation of Sirt1. Also, activation of Sirt1 by RES was shown to promote binding to PPARγ which repressed MSC differentiation into adipocytes. Additionally, RES suppresses osteoclastogenesis by acting through Sirt1 to bind to RANK which inhibited binding to RANKL”<-many of these processes should impact longitudinal bone growth as well.
Resveratrol stimulated tibial and vertabral length in new zealand white rabbits that were 12 weeks old. 200mg per kg of bodyweight were given. Increased the amount of chondrocytes in the tibia and stimulated growth plate area while reducing fusion. Decreased vascularization indicated by lower VEGF and laminin levels.
“RES supplementation delayed growth plate fusion by suppressing the replacement of avascular cartilage with vascularized bone indicated by the down-regulated gene expression of vascular endothelial growth factor, a signaling molecule in vascularization, and laminin, a cartilage protein.”
In 6 month old Fisher-Brown Norway rats, it increased tibia length and width. Dosage was 12.5mg per kg of bodyweight.
“In vitro, RES treatment of chondrocytes obtained from an adult rat femur protected against the catabolic effect of pro-inflammatory cytokine, interleukin-1β”