The soy isoflavone genistein inhibits the reduction in<scp>A</scp>chilles tendon collagen content induced by ovariectomy in rats

Ramos, Jahir E.; Al‐Nakkash, Layla; Peterson, Amity; Gump, Brian; Janjulia, Tea; Moore, Miranda S.; Carroll, Chad C.

doi:10.1111/j.1600-0838.2012.01516.x

Cited by 17 publications

(17 citation statements)

References 52 publications

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“…It should be clarified in future studies whether the changes observed in aged female mice are also present in aged male mice. Additionally, it has been suggested that treatment with phytoestrogens and exercise loading are effective for the maintenance of tendon mass and mechanical properties (35,36). Therefore, it would be important to determine whether phytoestrogens and exercise suppress and exhibit protective actions on the aging-associated decrease in the expression of collagen and tenogenic markers observed in the present study.…”

Section: Discussionmentioning

confidence: 83%

“…Stenosing tenosynovitis is a common tendinopathy in flexor tendons, and females are 6 times more likely to be affected compared with males (33,34). In addition, a previous study demonstrated that estrogen exhibits a protective effect on the tendon extracellular matrix, in particular collagen synthesis in females (35). Therefore, in the present study, to evaluate the aging-associated changes in tendons, postmenopausal female mice (78 weeks of age) were utilized.…”

Section: Discussionmentioning

confidence: 99%

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Effect of aging on the tendon structure and tendon‑associated gene expression in mouse foot flexor tendon

et al. 2019

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To evaluate the biological changes in tendons during the aging process, the present study examined the effect of aging on the tendon structure, distribution of collagen types I and III, and expression of tendon-associated genes, using flexor tendons in a mouse model. Histological assessment of the tendon structure and distribution of collagen types I and III were performed, and the expression of tendon-associated genes was evaluated in flexor digitorium longus tendons of young (8 weeks) and aged (78 weeks) female C57BL/6 mice. The results indicated that the Soslowsky score, based on the analysis of cellularity, fibroblastic changes, and collagen fiber orientation and disruption, was significantly increased, or worsened, in the tendons of the aged group compared with those in the young group. Furthermore, in the aged group, the distribution of type I collagen was decreased and the distribution of type III collagen was relatively increased compared with the young group. Finally, the mRNA expression levels of collagen (type I and type III) and tenogenic markers (Mohawk homeobox, tenomodulin and scleraxis BHLH transcription factor) were significantly decreased in the aged group compared with the young group. The present observations demonstrated that the structure of the tendons, distribution of types I and III collagen and the expression of tendon-associated genes were modulated by aging in the flexor tendon, and that these changes may contribute to the degeneration of tendons in tendinopathy.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Effect of aging on the tendon structure and tendon‑associated gene expression in mouse foot flexor tendon

et al. 2019

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“…HPLC. Patellar tendon collagen content was determined via quantification of hydroxyproline via fluorometric detection, as previously described with minor modifications (10,11,28). After derivatization, samples were injected onto a HPLC instrument (LC-20AB and SIL-20, Shimadzu Scientific Instruments, Columbia, MD).…”

Section: Methodsmentioning

confidence: 99%

“…Hydroxylyslpyridinoline (HP) cross-linking content was determined as previously described (10,11,28). A 500-l aliquot of the hydrolyzed sample was evaporated to dryness overnight at ambient temperature (Thermo Fisher Savant SPD131DDA SpeedVac Concentrator).…”

Section: Methodsmentioning

confidence: 99%

Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties

Volper

Huynh

Arthur

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Diabetes is a major risk factor for tendinopathy, and tendon abnormalities are common in diabetic patients. The purpose of the present study was to evaluate the effect of streptozotocin (60 mg/kg)-induced diabetes and insulin therapy on tendon mechanical and cellular properties. Sprague-Dawley rats (n = 40) were divided into the following four groups: nondiabetic (control), 1 wk of diabetes (acute), 10 wk of diabetes (chronic), and 10 wk of diabetes with insulin treatment (insulin). After 10 wk, Achilles tendon and tail fascicle mechanical properties were similar between groups (P > 0.05). Cell density in the Achilles tendon was greater in the chronic group compared with the control and acute groups (control group: 7.8 ± 0.5 cells/100 μm(2), acute group: 8.3 ± 0.4 cells/100 μm(2), chronic group: 10.9 ± 0.9 cells/100 μm(2), and insulin group: 9.2 ± 0.8 cells/100 μm(2), P < 0.05). The density of proliferating cells in the Achilles tendon was greater in the chronic group compared with all other groups (control group: 0.025 ± 0.009 cells/100 μm(2), acute group: 0.019 ± 0.005 cells/100 μm(2), chronic group: 0.067 ± 0.015, and insulin group: 0.004 ± 0.004 cells/100 μm(2), P < 0.05). Patellar tendon collagen content was ∼32% greater in the chronic and acute groups compared with the control or insulin groups (control group: 681 ± 63 μg collagen/mg dry wt, acute group: 938 ± 21 μg collagen/mg dry wt, chronic: 951 ± 52 μg collagen/mg dry wt, and insulin group: 596 ± 84 μg collagen/mg dry wt, P < 0.05). In contrast, patellar tendon hydroxylysyl pyridinoline cross linking and collagen fibril organization were unchanged by diabetes or insulin (P > 0.05). Our findings suggest that 10 wk of streptozotocin-induced diabetes does not alter rat tendon mechanical properties even with an increase in collagen content. Future studies could attempt to further address the mechanisms contributing to the increase in tendon problems noted in diabetic patients, especially since our data suggest that hyperglycemia per se does not alter tendon mechanical properties.

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“…One unit of insulin was administered subcutaneously twice a week or as desired. The dose of genistein was chosen based on recent published studies showing that genistein at 300 mg/kg was useful as pharmacological approach for the treatment of diabetic-induced cardiomyopathy [28][29][30]. The body weight of the rats was measured weekly using sensitive digital balance.…”

Section: Experimental Groupsmentioning

confidence: 99%

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

et al. 2015

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The present study was undertaken to evaluate the protective effects of genistein against cardiac inflammation and oxidative stress in streptozotocin (STZ) (45 mg/kg body weight)-induced diabetic rats. genistein (300 mg/kg/day) was administered orally for 24 weeks to STZ-induced diabetic rats. The effects of genistein on blood glucose, % glycosylated hemoglobin (HbA1c), C-reactive protein, tumor necrosis factor (TNF- α), transforming growth factor (TGF-β1), and total antioxidant were studied. Ultrastructural and histopathological assessment of injury were also undertaken using transmission electron microscope. STZ-induced diabetes resulted in significant increase in the levels of blood glucose, HbA1c, C-reactive protein, TNF- α and TGF-β1, and a decline in total antioxidant reserve of the myocardium. Administration of genistein to diabetic rats resulted in a decrease in blood glucose (p< 0.001), % HbA1c (p < 0.0001), C-reactive protein (p < 0.001), and expression of TNF- α (p < 0.001) and TGF-β1 (p < 0.0001) proteins. In addition, genistein treatment results in augmentation of total antioxidant (p < 0.01) reserve of the hearts. The above findings were supported by histological as well as immunohistochemical localization of NF-κB (p65) in the heart. Genistein treatment ameliorated the ultrastructural degenerative changes in the cardiac tissues as compared to the diabetic control. The result demonstrates that genistein restored the integrity of the diabetic myocardium by virtue of its anti-inflammatory and antioxidant effects.

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The soy isoflavone genistein inhibits the reduction inAchilles tendon collagen content induced by ovariectomy in rats

Cited by 17 publications

References 52 publications

Effect of aging on the tendon structure and tendon‑associated gene expression in mouse foot flexor tendon

Effect of aging on the tendon structure and tendon‑associated gene expression in mouse foot flexor tendon

Influence of acute and chronic streptozotocin-induced diabetes on the rat tendon extracellular matrix and mechanical properties

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

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