Monotropein attenuates oxidative stress via Akt/mTOR-mediated autophagy in osteoblast cells

Shi, Yao; Liu, Xiaoyan; Jiang, Yi-Ping; Zhang, Jiabao; Zhang, Qiaoyan; Wang, Nani; Xin, Hailiang

doi:10.1016/j.biopha.2019.109566

Cited by 38 publications

(19 citation statements)

References 22 publications

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“…He et al (15) demonstrated that Mtp attenuates inflammatory impairment on osteoblasts via inactivation of the nF-κB signaling pathway. Moreover, Mtp suppresses il-1β-induced apoptosis and catabolic responses on osteoarthritis chondrocytes (24), and in Mtp-treated osteoblasts, oxidative stress was alleviated via akt/mTor-mediated autophagy (11). However, the role of Mtp on endothelial cells in cVd has not been previously reported.…”

Section: Discussionmentioning

confidence: 94%

“…Monotropein (Mtp) is an iridoid glycoside isolated from the roots of Morinda officinalis (10). a previous study demonstrated that Mtp protected osteoblasts from H 2 o 2 -induced oxidative stress via regulating autophagy (11). Mtp induced the differentiation of bone marrow-derived endothelial progenitor cells and prevented cell apoptosis by decreasing the release of reactive oxygen species (roS) (12).…”

Section: Introductionmentioning

confidence: 99%

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Monotropein alleviates H2O2‑induced inflammation, oxidative stress and apoptosis via NF‑κB/AP‑1 signaling

Jiang

et al. 2020

Mol Med Rep

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aging is a major risk factor in cardiovascular disease (CVD). Oxidative stress and inflammation are involved in the pathogenesis of cVd, and are closely associated with senescent vascular endothelial cells. Monotropein (Mtp) exerts various bioactive roles, including anti-inflammatory and antioxidative effects. The aim of the present study was to investigate the function of Mtp in senescent endothelial cells. An MTT assay was performed to evaluate the influence of Mtp on H 2 o 2-stimulated human umbilical vein endothelial cells (HuVecs). Senescent cells were assessed by determining the expression of senescence-associated β-galactosidase, high mobility group aT-hook 1 and dna damage marker γ-H2a.X variant histone. Malondialdehyde (Mda), superoxide dismutase (Sod), glutathione peroxidase (GSH-Px) and proinflammatory cytokine concentrations were estimated using assay kits to evaluate the levels of oxidative stress and inflammation in HUVECs. The TUNEL assay was performed to identify apoptotic cells. Furthermore, the expression levels of endothelial cell adhesion factors, nF-κB, activator protein-1 (aP-1) and apoptotic proteins were determined via western blotting. Mtp enhanced HuVec viability following H 2 o 2 stimulation. H 2 o 2-mediated increases in Mda, proinflammatory cytokine and endothelial cell adhesion factor levels were decreased by Mtp treatment, whereas Mtp reversed H 2 o 2-mediated downregulation of Sod and GSH-Px activity. Furthermore, Mtp inhibited cell apoptosis, nF-κB activation and aP-1 expression in H 2 o 2-stimulated HuVecs; however, nF-κB activator counteracted the anti-inflammatory, antioxidative and antiapoptotic effects of Mtp. The present study indicated that Mtp ameliorated H 2 o 2-induced inflammation and oxidative stress potentially by regulating nF-κB/aP-1.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Monotropein alleviates H2O2‑induced inflammation, oxidative stress and apoptosis via NF‑κB/AP‑1 signaling

Jiang

et al. 2020

Mol Med Rep

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“…Oxidative stress and ROS are also fundamental in osteoblasts, and many previous studies verified the bone anabolic activities of natural products by using these targets [ 90 , 91 , 92 , 93 ]. Additionally, osteoblast studies also have also looked at alternative pathways such as Wnt/β-catenin to investigate the impairment or the amelioration of osteogenic potential [ 94 , 95 , 96 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Osteoporosis Effect of Perilla frutescens Leaf Hexane Fraction through Regulating Osteoclast and Osteoblast Differentiation

et al. 2022

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Osteoporosis is the result of an imbalance in the bone-remodeling process via an increase in osteoclastic activity and a decrease in osteoblastic activity. Our previous studies have shown that Perilla frutescens seed meal has anti-osteoclastogenic activity. However, the role of perilla leaf hexane fraction (PLH) in osteoporosis has not yet been investigated and reported. In this study, we aimed to investigate the effects of PLH in osteoclast differentiation and osteogenic potential using cell-based experiments in vitro. From HPLC analysis, we found that PLH contained high luteolin and baicalein. PLH was shown to inhibit RANKL-induced ROS production and tartrate-resistant acid phosphatase (TRAP)-positive multi-nucleated osteoclasts. Moreover, PLH significantly downregulated the RANKL-induced MAPK and NF-κB signaling pathways, leading to the attenuation of NFATc1 and MMP-9 expression. In contrast, PLH enhanced osteoblast function by regulating alkaline phosphatase (ALP) and restoring TNF-α-suppressed osteoblast proliferation and osteogenic potential. Thus, luteolin and baicalein-rich PLH inhibits osteoclast differentiation but promotes the function of osteoblasts. Collectively, our data provide new evidence that suggests that PLH may be a valuable anti-osteoporosis agent.

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“…Being a classical signal transduction pathway, the AKT/mTOR greatly affects the autophagic activity [ 28 – 30 ] and plays a vital role in the regulation of osteogenic differentiation [ 28 ]. In particular, mTOR is a negative regulator of autophagy initiation that can block the activation of Atg 1 kinase [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Paeoniflorin Attenuates Dexamethasone-Induced Apoptosis of Osteoblast Cells and Promotes Bone Formation via Regulating AKT/mTOR/Autophagy Signaling Pathway

Yang

Liu

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Paeoniflorin, a natural product derived from Paeonia lactiflora, possesses diverse pharmacological activities such as anti-inflammatory, antitumor, and antidiabetic effects. It has been reported for promoting osteoblastogenesis and inhibiting osteoclastogenesis. This study investigates the therapeutic effects of paeoniflorin in glucocorticoid-induced osteoporosis (GIOP) in vitro and in vivo. MC3T3-E1 cells were incubated with dexamethasone (DEX; 200 μM) and/or paeoniflorin (10 μM), followed by the investigation of cell proliferation, differentiation, mineralization, apoptosis, and autophagy. The AKT activator SC79 was used for evaluating the involvement of the AKT/mTOR signaling pathway. After DEX pretreatments, paeoniflorin promoted osteoblast differentiation and mineralization characterized by increase in Runx2, ALP, beclin-1, and LC3-II/LC3-I ratio levels and a decrease in apoptosis. The autophagy-promoting effects of paeoniflorin were reversed by SC79. C57BL/6 mice were given DEX (1 mg/kg) once daily and paeoniflorin (15 mg/kg) 48 hours for a total of 8 weeks followed by the investigation of histological changes, the trabecular bone microarchitecture, and the levels of bone turnover markers. The results showed that paeoniflorin increased alkaline phosphatase (ALP) activity and upregulated the expression of osteocalcin and beclin-1 but reduced the levels of Bax and C-terminal telopeptide of type I collagen (CTX-1). Thus, paeoniflorin may alleviate DEX-induced osteoporosis by promoting osteogenic differentiation and autophagy via inhibition of the AKT/mTOR signaling pathway.

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Monotropein attenuates oxidative stress via Akt/mTOR-mediated autophagy in osteoblast cells

Cited by 38 publications

References 22 publications

Monotropein alleviates H2O2‑induced inflammation, oxidative stress and apoptosis via NF‑κB/AP‑1 signaling

Monotropein alleviates H2O2‑induced inflammation, oxidative stress and apoptosis via NF‑κB/AP‑1 signaling

Anti-Osteoporosis Effect of Perilla frutescens Leaf Hexane Fraction through Regulating Osteoclast and Osteoblast Differentiation

Paeoniflorin Attenuates Dexamethasone-Induced Apoptosis of Osteoblast Cells and Promotes Bone Formation via Regulating AKT/mTOR/Autophagy Signaling Pathway

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