Puerarin inhibits TRPM3/miR‐204 to promote MC3T3‐E1 cells proliferation, differentiation and mineralization

Zeng, Xiangwei; Qian, Feng; Zhao, Fu-Jun; Sun, Chao; Zhou, Tao; Yang, Jing; Zhan, Xiaoli

doi:10.1002/ptr.6034

Cited by 31 publications

(20 citation statements)

References 20 publications

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“…Puerarin([8‐(β‐ d ‐glucopyranosyl‐7‐hydroxy‐3‐(4‐hydroxyphenyl)‐4H‐1‐benzopyran‐4‐one]) is a major bioactive isoflavone compound isolated from the roots of the Pueraria lobata and has been clinically used for its protection against inflammation, oxidative stress, and mitochondrial dysfunction (Wang, Shi, et al, ; Zeng et al, ). It is reported that puerarin might be beneficial to improve lipid metabolism (Prasain, Peng, Rajbhandari, & Wyss, ), restore mitochondrial function (Song, Liu, Wang, & Wang, ), and meliorate glucose homeostasis (Yang et al, ).…”

Section: Introductionmentioning

confidence: 99%

Puerarin protects against high‐fat high‐sucrose diet‐induced non‐alcoholic fatty liver disease by modulating PARP‐1/PI3K/AKT signaling pathway and facilitating mitochondrial homeostasis

Wang

Yang

Shang

et al. 2019

Phytotherapy Research

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As yet, there was no effective pharmacological therapy approved for non‐alcoholic fatty liver disease (NAFLD). Here, we aimed to evaluate the therapeutic potential of puerarin against NAFLD and explored the underlying mechanisms. C57BL/6J mice were fed with a high‐fat high‐sucrose (HFHS) diet with or without puerarin coadministration intragastrically. The levels of hepatocellular injury, steatosis, fibrosis, and mitochondrial and metabolism alteration were detected. First, puerarin ameliorated histopathologic abnormalities due to HFHS. We observed a marked increase in hepatic lipid content, inflammation, and fibrosis level, which were attenuated by puerarin. Possible mechanisms were related to puerarin‐mediated activation of PI3K/AKT pathway and further improvement in fatty acid metabolism. Puerarin restored the NAD+ content and beneficially affected the hepatic mitochondrial function, which attenuated HFHS‐induced steatosis and metabolic disturbances. Finally, hepatic PARP‐1 was activated due to excessive fat intake. Puerarin attenuated the PARP‐1 expression in HFHS‐fed mice, and PJ34, the PARP inhibitor, could mimic these protections of puerarin. However, pharmacological inhibition of PI3K disabled the protection of puerarin or PJ34 toward NAD+ refilling and mitochondrial homeostasis. In conclusion, our findings indicated that puerarin could be a promising and practical therapeutic strategy in NAFLD through modulating PARP‐1/PI3K/AKT signaling pathway and further facilitating mitochondrial function.

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Section: Introductionmentioning

confidence: 99%

Puerarin protects against high‐fat high‐sucrose diet‐induced non‐alcoholic fatty liver disease by modulating PARP‐1/PI3K/AKT signaling pathway and facilitating mitochondrial homeostasis

Wang

Yang

Shang

et al. 2019

Phytotherapy Research

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“…Puerarin, an isoflavone extracted from the Chinese medicine pueraria, exhibits protective functions on the cardiovascular system, nervous system, osteoporosis, liver injury, and inflammation in vivo and in vitro (4). Studies have shown that puerarin can promote the proliferation, differentiation and mineralization of osteoblasts in vitro (5,6). In a recent report, puerarin was found to improve bone loss in estrogen-deficient rats, display a superior anti-osteoporosis effect, and prevent osteoporosis in postmenopausal women (7).…”

Section: Introductionmentioning

confidence: 99%

“…To date, LC3B has been extensively studied and identified as an autophagic membrane-associated factor (13). Previous studies have demonstrated that a low concentration of puerarin can promote the viability and differentiation of osteoblastic MC3T3-E1 cells, which may be achieved by downregulation of the expression of miR-204 and its host gene TRPM3 (6). However, it is not clear whether there are other targets in this pathway.…”

Section: Introductionmentioning

confidence: 99%

Puerarin promotes the viability and differentiation of MC3T3‑E1 cells by enhancing LC3B‑mediated autophagy through downregulation of miR‑204

et al. 2019

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Puerarin is a bioactive substance extracted from Pueraria lobata. It is known to promote the viability, differentiation and mineralization of osteoblasts. However, the molecular mechanisms involved in these activities are not well understood. The present study was conducted with the aim of elucidating the effect of puerarin on osteoblasts and to explore the underlying mechanism. CCK-8 analysis showed that puerarin (0.1, 1 and 10 µM) promoted the viability of osteoblastic MC3T3-E1 cells, with 1 µM of puerarin exhibiting the strongest effect. Moreover, 1 µM puerarin significantly increased the activity of alkaline phosphatase (ALP) and the formation of mineralized nodules in the MC3T3-E1 cells. Treatment with 1 µM puerarin for 72 h led to a significant upregulation in the expression level of microtubule-associated light chain 3 (LC3)B and Beclin1 proteins. This treatment was more effective in promoting LC3B expression than what was observed following treatment with rapamycin (overexpression for autophagy). The bilayer membrane structure of autophagosomes was observed by electron microscopy. Conversely, 3-methyladenine (3-MA, inhibitor of autophagy) reduced the cell viability as well as the activity of alkaline phosphatase (ALP) in MC3T3-E1 cells, although, there was no significant influence on mineralization. Prediction results of the biological information showed that LC3B could be a direct target of . In the present study, the expression level of miR-204 was decreased by puerarin. miR-204 mimics significantly decreased LC3B expression and inhibited auotophagosome formation, while the miR-204 inhibitor had the opposite effects. To conclude, the results of the present study suggest that puerarin promotes the viability and differentiation of MC3T3-E1 cells through autophagy, which is possibly associated with miR-204-regulated LC3B upregulation.

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“…12). Mineralization is a critical biological characteristic of osteoblasts (36). The results showed a satisfactory mineralization function of the cultured osteoblasts.…”

Section: F-actin Staining In Cells Pretreated With Rock1 Inhibitor Y-mentioning

confidence: 86%

Low‑dose X‑ray irradiation induces morphological changes and cytoskeleton reorganization in osteoblasts

et al. 2020

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Recently, research into the biological effects of low dose X-ray irradiation (LDI) has been a focus of interest. Numerous studies have suggested that cells exhibit different responses and biological effects to LDI compared with high doses. Preliminary studies have demonstrated that LDI may promote osteoblast proliferation and differentiation in vitro, thereby accelerating fracture healing in mice. However, the exact mechanism of action by which LDI exerts its effects remains unclear. Previous studies using microarrays revealed that LDI promoted the expression of genes associated with the cytoskeleton. In the current study, the effect of X-ray irradiation (0.5 and 5 Gy) on the morphology of MC3T3-E1 cells and fiber actin organization was investigated. Osteoblasts were treated with 0, 0.5 and 5 Gy X-ray irradiation, following which changes in the actin cytoskeleton were observed. The levels of RhoA, ROCK, cofilin and phosphorylated-cofilin were measured by reverse transcription-quantitative PCR and western blotting. Subsequently, osteoblasts were pretreated with ROCK specific inhibitor Y27632 to observe the changes of actin skeleton after X-ray irradiation. The results demonstrated that the cellular morphological changes were closely associated with radiation dose and exposure time. Furthermore, the gene expression levels of small GTPase RhoA and its effectors were increased following LDI. These results indicated that the RhoA/Rho-associated kinase pathway may serve a significant role in regulating LDI-induced osteoblast cytoskeleton reorganization.

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Puerarin inhibits TRPM3/miR‐204 to promote MC3T3‐E1 cells proliferation, differentiation and mineralization

Cited by 31 publications

References 20 publications

Puerarin protects against high‐fat high‐sucrose diet‐induced non‐alcoholic fatty liver disease by modulating PARP‐1/PI3K/AKT signaling pathway and facilitating mitochondrial homeostasis

Puerarin protects against high‐fat high‐sucrose diet‐induced non‐alcoholic fatty liver disease by modulating PARP‐1/PI3K/AKT signaling pathway and facilitating mitochondrial homeostasis

Puerarin promotes the viability and differentiation of MC3T3‑E1 cells by enhancing LC3B‑mediated autophagy through downregulation of miR‑204

Low‑dose X‑ray irradiation induces morphological changes and cytoskeleton reorganization in osteoblasts

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