Tanshinol Alleviates Osteoporosis and Myopathy in Glucocorticoid-Treated Rats

Abstract

Tanshinol is a major water-soluble active component of . In this study, we aimed to investigate whether tanshinol has potential therapeutic effects against glucocorticoid-induced osteoporosis and glucocorticoid-induced myopathy. Ninety-six female Sprague-Dawley rats were randomly assigned to five groups: a control group, a model group, and three model groups treated with 25 or 50 mg/kg of tanshinol, or calcitriol. All model groups received prednisone acetate for 90 days to induce glucocorticoid-induced osteoporosis. Afterwards, all animals underwent a surgical procedure to induce bone defects at the right proximal tibia. Prednisone treatment was stopped after surgery, but tanshinol or calcitriol treatment was continued to the endpoint. At the experimental endpoint, compared to the model group, 25 mg/kg tanshinol could significantly reverse glucocorticoid-induced loss of bone mineral density by 12.5 %, while enhancing mechanical bone strength, causing a significant 11 % increase in trabecular number, and reducing trabecular separation by 28 %. In addition, tanshinol improved the bone microarchitecture and prevented glucocorticoid-induced bone loss by promoting bone formation and inhibiting bone resorption. Moreover, results of bone defect repair and muscle weight measurements revealed that tanshinol accelerated the bone fracture healing process and attenuated muscle atrophy caused by glucocorticoid. Furthermore, qRT-PCR analysis showed a 1-fold upregulation in mRNA levels of transforming growth factor beta and roughly 6-fold increases in vascular endothelial growth factor mRNA expression in calluses from the tanshinol groups. Tanshinol also preserved muscular ubiquitin mRNA levels from glucocorticoid-induced elevation. These findings demonstrate the potential benefits of tanshinol against glucocorticoid-induced osteoporosis and glucocorticoid-induced myopathy, which warrants further investigation in future studies.

Plant Extracts in the Bone Repair Process: A Systematic Review

“…Only 25.81% ( n = 8) [28, 32, 35, 38, 39, 43, 46, 50] performed measurement of inflammatory markers, and the most cited parameters were Ca +2 content and serum alkaline phosphatase. Only 25.81% ( n = 8) [22, 32, 37, 38, 42, 46, 48, 49] reported whether the fracture had complete, partial, or absent closure. Other analyses related to bone strength, tensile strength, and expression of inflammatory genes that stimulate bone formation and osteogenic differentiation were performed in 38.71% ( n = 12) of the studies [20, 23, 24, 28, 33, 36, 40–42, 44, 45, 47] (Figure 2).…”

Retracted: Tanshinol relieves lipopolysaccharide‐induced inflammatory injury of HaCaT cells via down‐regulation of microRNA‐122

“…(Lamiaceae; Y. Yang et al, ). Pharmacological researches have demonstrated that TAN exerts multiple beneficial biological activities, such as antioxidation (Y. Yang et al, ), antiliver fibrosis (Peng et al, ), antiosteoporosis (Chen et al, ), antiatherosclerosis (Song, Pu, & He, ), and anti‐inflammation (Y. Yang et al, ). In terms of anti‐inflammatory activity, Y. Yang et al () reported that TAN inhibited inflammatory response in a rat model of vascular dementia.…”

<p>Bone-Targeting Liposome-Encapsulated Salvianic Acid A Improves Nonunion Healing Through the Regulation of HDAC3-Mediated Endochondral Ossification</p>

“…Earlier reports have shown that SAA stimulates osteogenesis and depresses adipogenesis in BMSCs both in vitro and in vivo. 15,16,43 Specifically, SAA attenuates the impairment of bone formation, bone loss, and bone quality deterioration elicited by glucocorticoid-mediated KLF15/WNT signalling and suppresses the glucocorticoid-induced oxidative stress and subsequent cell apoptosis associated with the KLF15/p66Shc signalling cascade. 17 Yang et al confirmed the protective effects of SAA on oxidative stress and its signalling pathways in osteoblastic differentiation.…”

“…Several studies have shown that SAA stimulates osteogenesis and angiogenesis by regulating WNT signalling and oxidative stress. [14][15][16][17][18] However, the specific mechanism of SAA employed to accelerate fracture healing has not yet been fully elucidated. Relatively few studies have focused on the role of chondrogenesis, which involves the formation of cartilage that facilitates an initial union of most long bone fractures, 6,19 or endochondral ossification, which plays a vital role in the process of bone tissue repair during long bone fracture.…”