Tanshinone <scp>IIA</scp> treatment alleviated the rat gingival connective tissue overgrowth induced by cyclosporine A

Ma, Sisi; Liu, W; Liu, P; Liu, J; Chen, L; Qin, Chunlin

doi:10.1111/jre.12335

Cited by 5 publications

(4 citation statements)

References 40 publications

(89 reference statements)

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“…The pharmacological and therapeutic properties of Tan-IIA in the cardiovascular system have attracted interest ( 12 ). A previous study showed that Tan-IIA treatment alleviated rat gingival connective tissue overgrowth induced by cyclosporine A ( 13 ). Emerging experimental investigations and clinical trials have demonstrated that Tan-IIA prevents cardiac injury, hypertrophy and atherogenesis through estrogen receptor-α-induced oxidative stress ( 14 ).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone‑IIA attenuates the deleterious effects of oxidative stress in osteoporosis through the NF‑κB signaling pathway

et al. 2018

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Osteoclasts are responsible for bone resorption caused by bone microstructural damage and bonerelated disorders. Evidence shows that tanshinone IIA (Tan-IIA), a traditional Chinese medicine, is used clinically as a drug for the treatment of cardiovascular and cerebrovascular diseases. However, the efficacy and mechanism underlying the effect of Tan-IIA on the viability of osteoclasts remain to be fully elucidated. The present study investigated the therapeutic effects of Tan-IIA on osteoblast differentiation and oxidative stress in vitro and in vivo. Cell viability was analyzed and oxidative stress was examined in the osteoblasts. Wnt1sw/sw mice were used to investigate the therapeutic effects of Tan-IIA on spontaneous tibia fractures and severe osteopenia. The bone strength, collagen and mineral were examined in the tibia. Osteoblast activity was also analyzed in the experimental mice. The Tan-IIA-induced differentiation of osteoclasts and the mechanism of action were investigated in osteocytes. The data showed that Tan-IIA treatment improved cell viability. The data also demonstrated that Tan-IIA decreased the levels of H2O2, accumulation of reactive oxygen species and apoptosis of osteoblasts. Tan-IIA inhibited the deleterious outcomes triggered by oxidative stress. In addition, Tan-IIA inhibited the activation of nuclear factor (NF)-κB and its target genes, tumor necrosis factor (TNF)-α, inducible nitric oxide synthase and cyclooxygenase 2, and increased the levels of TNF receptor-associated factor 1 and inhibitor of apoptosis protein-1/2 in the osteocytes. Furthermore, it was shown that Tan-IIA reduced the propensity to fractures and severe osteopenia in mice with osteoporosis. Tan-IIA also exhibited improved bone strength, mineral and collagen in the bone matrix of the experimental mice. It was found that the Tan-IIA-mediated benefits on osteoblast activity and function were through the NF-κB signaling pathway. Taken together, the data obtained in the present study suggested that Tan-IIA had protective effects against oxidative stress in osteoblastic differentiation in mice with osteoporosis by regulating the NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Tanshinone‑IIA attenuates the deleterious effects of oxidative stress in osteoporosis through the NF‑κB signaling pathway

et al. 2018

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“…36 In addition, it was not observed in this study that the cyclosporine A administration altered the TGFβ1. Previous studies have shown an ambiguous effects of the cyclosporine A on TGFβ1 expression since it was showed that the cyclosporine A increased the TGFβ1expression in inflamed gingiva, 37 and reduced the TGFβ1expression in human lung fibroblasts. 38 This dual effect of the cyclosporine A observed in these different inflammatory conditions may be the reason of the absence of the interference of this drug on the TGFβ1expression in the model used in this study.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporine A impairs bone repair in critical defects filled with different osteoconductive bone substitutes

et al. 2020

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The aim of this study was to assess the influence of cyclosporine administration on the repair of critical-sized calvaria defects (CSDs) in rat calvaria filled with diverse biomaterials. Sixty animals were divided into two groups: the control (CTR) group (saline solution) and the cyclosporine (CCP) group (cyclosporine, 10 mg/kg/day). These medications were administered daily by gavage, beginning 15 days before the surgical procedure and lasting until the day the animals were euthanized. A CSD (5 mm Ø) was made in the calvaria of each animal, which was allocated to one of 3 subgroups, according to the biomaterial used to fill the defect: coagulum (COA), deproteinized bovine bone (DBB), or biphasic calcium phosphate ceramics of hydroxyapatite and β-phosphate tricalcium (HA/TCP). Euthanasia of the animals was performed 15 and 60 days after the surgical procedure (n = 5 animals/period/ subgroup). Bone repair (formation) assessment was performed through microtomography and histometry, while the analyses of the expression of the BMP2, Osteocalcin, and TGFβ1 proteins were performed using immunohistochemistry. The CSDs not filled with biomaterials demonstrated lower bone formation in the CCP group. At 15 days, less bone formation was observed in the CSDs filled with DBB, a smaller volume of mineralized tissue was observed in the CSDs filled with HA/TCP, and the expression levels of BMP2 and osteocalcin were lower in the CCP group compared to the CTR group. The use of cyclosporine impaired bone repair in CSD, and this effect can be partially explained by the suppression of BMP2 and osteocalcin expression.

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“…Except for the suppressive effects on TIMP1 and TIMP4 via the induction of miR-618, the direct interaction between TAN and TIMPs is also widely reported. For instance, the study by Ma et al (2016) showed that TAN treatment alleviates the rat gingival connective tissue overgrowth via the inhibition of TIMP1. Moreover, the study by Tsai (2011) indicated that TAN can also attenuate high glucoseinduced collagen synthesis via by suppressing TIMP4 level in CFs.…”

Section: Discussionmentioning

confidence: 99%

“…Yang et al (2015) indicated that TAN exerts antifibrotic effects in myocardial tissues by inducing the level of miR-29b. Moreover, TAN also shows suppressive effects on TIMP family members such as TIMP1 (Ma et al, 2016) and TIMP2 (Tsai, 2011). Thus, TAN is a promising cardioprotective compound, and its antifibrotic effect may be closely related to the function of miRs.…”

Section: Introductionmentioning

confidence: 96%

Tanshinone IIA fromSalvia miltiorrhizaexerts anti‐fibrotic effects on cardiac fibroblasts and rat heart tissues by suppressing the levels of pro‐fibrotic factors: The key role of miR‐618

Yan

Xiao

Wang

et al. 2022

Journal of Food Biochemistry

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Tanshinone IIA (TAN) is widely employed for handling cardiovascular disorders. The current study explored the potential role of miRs in the antifibrotic effect of TAN on heart. Fibrotic features were induced in cardiac fibroblasts (CFs) and in rat hearts, and then handled with TAN. MicroRNAs (miRs) responding to TAN were determined using a microarray assay. The selected miR was modulated to verify its role in antifibrotic effects of TAN. TAN suppressed the viability and the production of α-SMA in CFs, which was associated with 101 miR being upregulated and 223 miR being downregulated. MiR-618 was selected as the potential target of TAN. Ang II inhibited miR-618 level and resulted in the upregulation of pro-fibrosis factors, which was reversed by TAN. The antifibrotic effect of TAN was weakened by miR-618 inhibition. TAN inhibits hypertrophy and collagen deposition in heart tissues, which is associated with the increased level of miR-618. Practical applicationsThe findings outlined in the current study show that the antifibrotic function of TAN is closely related to the function of miRs: the induction of miR-618 is indispensable for the function of TAN against the fibrotic process after heart injury, which will promote the application of TAN as an adjuvant therapy for improving heart function.

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Tanshinone IIA treatment alleviated the rat gingival connective tissue overgrowth induced by cyclosporine A

Cited by 5 publications

References 40 publications

Tanshinone‑IIA attenuates the deleterious effects of oxidative stress in osteoporosis through the NF‑κB signaling pathway

Tanshinone‑IIA attenuates the deleterious effects of oxidative stress in osteoporosis through the NF‑κB signaling pathway

Cyclosporine A impairs bone repair in critical defects filled with different osteoconductive bone substitutes

Tanshinone IIA fromSalvia miltiorrhizaexerts anti‐fibrotic effects on cardiac fibroblasts and rat heart tissues by suppressing the levels of pro‐fibrotic factors: The key role of miR‐618

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