Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways

Lu, Junyan; Ye, Chenyi; Huang, Yanyong; Huang, Donghui; Tang, Lan; Hou, Weiduo; Kuang, Zhihui; Chen, Yazhou; Xiao, Shining; Yishake, Mumingjiang; He, Rongxin

doi:10.1111/jcmm.15657

Cited by 12 publications

(9 citation statements)

References 52 publications

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“…[32,33] Lu et al found that it has a significant negative impact of trap-positive osteoclasts at a concentration of 2 µmol/L, which is inconsistent with our results showing that Cor inhibits osteoclast differentiation at ≥5 µmol/L and Cor has no cytotoxicity on BMMs even at concentrations of up to 20 µmol/L. [34] This difference may be related to the plant source of the extracted Cor. Fangchinoline, ellagic acid, arctiin, and other drug monomers can affect osteoclast formation to inhibit osteoclast fusion, consistent with the effect of Cor on the function of osteoclasts.…”

Section: Discussioncontrasting

confidence: 99%

Corilagin attenuates osteoclastic osteolysis by enhancing HO‐1 and inhibiting ROS

Tan

Huang

et al. 2022

J Biochem & Molecular Tox

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Chinese herbal medicine has well‐established therapeutic effects in various diseases. Corilagin (Cor), a gallic acid tannin in Phyllanthus niruri L., has anti‐inflammatory and antioxidant effects in many diseases. However, its role in osteoclast‐related bone diseases has not been determined. In vitro, bone marrow macrophages (BMMs) were extracted and isolated to differentiate into osteoclasts. The effects of Cor on osteoclast formation, bone resorption, and reactive oxygen species (ROS) production were performed. In addition, quantitative real‐time polymerase chain reaction and western blot analysis were used to evaluate the effect of Cor on oxidative stress‐related pathways, which are nuclear factors‐κB ligand‐receptor activator (RANKL) stimulates important downstream pathways. Furthermore, microcomputed tomography and bone histomorphometry were performed to analyze the therapeutic effect of Cor in mouse models of lipopolysaccharide (LPS)‐mediated bone defects in vivo. Cor influenced the nuclear factor of activated T cells 1 (NFATc1) signaling pathway and reduced ROS in RANKL‐treated osteoclasts, thereby inhibiting osteoclast formation and bone resorption. Moreover, Cor protected against LPS‐mediated skull defects in vivo. In sum, our results confirm that Cor can inhibit osteoclastogenesis and intracellular oxidative stress. In addition, the inflammatory bone defect induced by LPS was also attenuated by Cor. Accordingly, Cor is a new candidate therapeutic agent for osteoclast‐mediated osteolytic diseases.

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Section: Discussioncontrasting

confidence: 99%

Corilagin attenuates osteoclastic osteolysis by enhancing HO‐1 and inhibiting ROS

Tan

Huang

et al. 2022

J Biochem & Molecular Tox

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“…Corilagin, a water-soluble tannin, is the primary bioactive ingredient of the E. phyllanthus plant. Corilagin possesses anti-viral, anti-inflammatory, antioxidant and antitumor properties (10)(11)(12). Corilagin inhibits proliferation of a variety of cancer cells, including hepatic carcinoma, as well as breast, gastric and ovarian cancer (15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

“…Corilagin is the primary active ingredient of the Euphorbia phyllanthus plant and has antiviral, anti-inflammatory, antioxidant and other biological activity (10)(11)(12). Corilagin can effectively diminish inflammation in ulcerative colitis and cystic fibrosis bronchial cells.…”

Section: Introductionmentioning

confidence: 99%

Corilagin induces apoptosis and inhibits autophagy of HL‑60 cells by regulating miR‑451/HMGB1 axis

Jia

Xiao

et al. 2021

Mol Med Rep

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Corilagin is the primary active component of the Euphorbia phyllanthus plant and has significant anti-cancer properties. However, the biological effects and mechanisms of corilagin on acute myeloid leukemia (AML) have not been clarified. The Cell Counting Kit-8 and Carboxyfluorescein Diacetate Succinimidyl Ester assay results showed that corilagin significantly inhibited proliferation of the AML cell line HL-60 in a time-and dose-dependent manner. Western blotting and flow cytometry analysis were performed to determine the levels of apoptosis in HL-60 cells. The protein levels of cleaved caspase-3 and Bak were upregulated, while Bcl-xl was downregulated in cells treated with corilagin. The percentage of early-and late-stage apoptotic cells increased following corilagin treatment in a dose-dependent manner, indicating that the intrinsic mitochondrial apoptosis pathway was activated by corilagin. Simultaneously, western blotting and immunofluorescence results revealed that autophagy was suppressed; this was accompanied by a decrease in light chain 3-II (LC3-II) conversion and autophagosomes. MicroRNA (miRNA/miR) profile analysis showed that corilagin elevated the expression of the tumor suppressor miR-451, while the mRNA and protein levels of high mobility group protein B1 (HMGB1), the target of miR-451, decreased following exposure to corilagin. Knockdown of miR-451 decreased the downregulation of HMGB1 caused by corilagin, indicating negative regulation of HMGB1 by miR-451 during corilagin treatment. Furthermore, knockdown of miR-451 also attenuated corilagin-induced proliferation inhibition of HL-60 cells, implying that miR-451 was essential for the proliferation inhibitory effect of corilagin. In conclusion, these results indicated that corilagin induced apoptosis and inhibited autophagy in HL-60 cells by regulating the miR-451/HMGB1 axis, and corilagin may be a novel therapeutic drug for the treatment of AML.

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“…LncRNA PTTG3P can promote the expression of CCND1 and PARP2 by competitively binding miR-383, thus affecting the PI3K/AKT signaling pathway to promote the growth and metastasis of HCC cells [ 53 ]. LncRNA MALAT1 and DLEU1 can promote the expression of EGFR and IGF-1R by acting as the ceRNA of miR-195 and miR-133a, respectively, thereby activating the downstream PI3K/Akt signaling pathway to accelerate the HCC progression [ 54 ]. The expression of PTEN was reported to be decreased in nearly half of all HCC tumors, leading to the activation of the PI3K/Akt/mTOR pathway to promote HCC tumorigenesis.…”

Section: The Lncrna-mediated Cerna Network (Cernets) Functions By Modulating Signaling Pathways In Hccmentioning

confidence: 99%

The role of ceRNA-mediated diagnosis and therapy in hepatocellular carcinoma

et al. 2021

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Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide due to its high degree of malignancy, high incidence, and low survival rate. However, the underlying mechanisms of hepatocarcinogenesis remain unclear. Long non coding RNA (lncRNA) has been shown as a novel type of RNA. lncRNA by acting as ceRNA can participate in various biological processes of HCC cells, such as tumor cell proliferation, migration, invasion, apoptosis and drug resistance by regulating downstream target gene expression and cancer-related signaling pathways. Meanwhile, lncRNA can predict the efficacy of treatment strategies for HCC and serve as a potential target for the diagnosis and treatment of HCC. Therefore, lncRNA serving as ceRNA may become a vital candidate biomarker for clinical diagnosis and treatment. In this review, the epidemiology of HCC, including morbidity, mortality, regional distribution, risk factors, and current treatment advances, was briefly discussed, and some biological functions of lncRNA in HCC were summarized with emphasis on the molecular mechanism and clinical application of lncRNA-mediated ceRNA regulatory network in HCC. This paper can contribute to the better understanding of the mechanism of the influence of lncRNA-mediated ceRNA networks (ceRNETs) on HCC and provide directions and strategies for future studies.

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Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways

Cited by 12 publications

References 52 publications

Corilagin attenuates osteoclastic osteolysis by enhancing HO‐1 and inhibiting ROS

Corilagin attenuates osteoclastic osteolysis by enhancing HO‐1 and inhibiting ROS

Corilagin induces apoptosis and inhibits autophagy of HL‑60 cells by regulating miR‑451/HMGB1 axis

The role of ceRNA-mediated diagnosis and therapy in hepatocellular carcinoma

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