Oleanolic acid induces autophagic death in human gastric cancer cells in vitro and in vivo

Nie, Hao; Wang, Yu; Qin, Yong; Gong, Xingguo

doi:10.1002/cbin.10612

Cited by 34 publications

(26 citation statements)

References 26 publications

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“…Increasing research reported that AMPK plays an important role in inflammation, and metformin can serve as a potential drug to treat inflammation‐related disorders. Adenosine 5′‐monophosphate‐activated protein kinase is activated by natural products, such as ginsenoside (Yao et al, ), oleanolic acid (Nie et al, ) and ursolic acid (Meng et al, ), all of which suppress the release of inflammatory cytokines in LPS‐induced ALI. It has been demonstrated that mogroside V and its aglycone (mogrol) are both potent AMPK activators (Chen et al, ; Harada et al, ; Luo et al, ).…”

Section: Resultsmentioning

confidence: 99%

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

Tao

Cao

et al. 2017

Phytotherapy Research

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Acute lung injury (ALI) often leads to high mortality, and there is as yet no effective drug treatment. The present study aimed to investigate protective effects of mogroside IIIE (MGIIIE, a cucurbitane-type triterpenoid from Siraitia grosvenorii Fruits) in experimental ALI and its underlying mechanism. MGIIIE (1, 10 0r 20 mg/kg) was orally administered for 1 h before a single intratracheal administration of lipopolysaccharide (LPS, 5 mg/kg). MGIIIE treatment dose-dependently suppressed pulmonary oedema, pro-inflammatory mediators (IL-1β, IL-6, TNF-α and HMGB1) release and higher MPO activity in lung tissues induced by LPS challenge. Molecular researches showed that mogroside IIIE (20 mg/kg) not only increased the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK) but suppressed the over-expression of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). In addition, MGIIIE also inhibited the activation of MAPKs and nuclear factor κB (NF-κB) signalling in lung tissues from LPS-challenged mice. Similar antiinflammatory effects of MGIIIE were obtained in LPS-treated macrophages. Compound C (a pharmacological AMPK inhibitor) obviously reversed the antiinflammatory effect of MGIIIE in LPS-induced ALI mice. Taken together, AMPK activation plays a crucial role in the antiinflammatory effects of MGIIIE in LPS-induced ALI by down-regulating TLR4/MAPK/NF-κB signalling pathways. Copyright © 2017 John Wiley & Sons, Ltd.

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Section: Resultsmentioning

confidence: 99%

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

Tao

Cao

et al. 2017

Phytotherapy Research

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“…In addition, over-expression of Akt also reversed the effects of oleanolic acid [60]. Importantly, oleanolic acid is also an inhibitor of extracellular signal–regulated kinase/c-Jun N-terminal kinase/mitogen-activated protein kinase (ERK/JNK/p38 MAPK) signaling pathway mediated by the activation of the 5′ adenosine monophosphate-activated protein kinase (AMPK) signaling pathway that consequently activates downstream signaling leading to the mTOR inhibition and activation of autophagy [55,68,73]. A significant decrease in p-p38α/p38α ratio and in the levels of p-JNK1 and pERK1/2 together with the increased phosphorylation of AMPK were reported in oleanolic acid-treated cancer cells [74].…”

Section: Oleanolic Acid As Anticancer Agentmentioning

confidence: 99%

“…Oleanolic acid derivative, SZC015, activated intrinsic apoptosis, as observed by the up-regulation of caspase-3 and caspase-9, poly (ADP-ribose) polymerase (PARP) cleavage, release of cytochrome c, as well as increase in Bax/Bcl-2 expression ratio [55,87]. Moreover, oleanolic acid and its derivatives also caused autophagy, i.e., formation of autophagic vacuoles, elevated microtubule-associated protein 1 light chain 3α (MAP1LC3A), increased LC3II/LC3I ratio and upregulated the expression of Atg5 and beclin1 in hepatic [50], breast [55] and gastric cancer cells [73,87]. Interestingly, oleanolic acid-triggered autophagy was ROS-dependent as shown by elevated cellular ROS levels, and the effect was abolished if ROS levels were reduced [50,62].…”

Section: Oleanolic Acid As Anticancer Agentmentioning

confidence: 99%

Oleanolic Acid Alters Multiple Cell Signaling Pathways: Implication in Cancer Prevention and Therapy

Žiberna

Šamec

Mocan

et al. 2017

IJMS

114

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Nowadays, much attention has been paid to diet and dietary supplements as a cost-effective therapeutic strategy for prevention and treatment of a myriad of chronic and degenerative diseases. Rapidly accumulating scientific evidence achieved through high-throughput technologies has greatly expanded the understanding about the multifaceted nature of cancer. Increasingly, it is being realized that deregulation of spatio-temporally controlled intracellular signaling cascades plays a contributory role in the onset and progression of cancer. Therefore, targeting regulators of oncogenic signaling cascades is essential to prevent and treat cancer. A plethora of preclinical and epidemiological evidences showed promising role of phytochemicals against several types of cancer. Oleanolic acid, a common pentacyclic triterpenoid, is mainly found in olive oil, as well as several plant species. It is a potent inhibitor of cellular inflammatory process and a well-known inducer of phase 2 xenobiotic biotransformation enzymes. Main molecular mechanisms underlying anticancer effects of oleanolic acid are mediated by caspases, 5 adenosine monophosphate-activated protein kinase, extracellular signal-regulated kinase 1/2, matrix metalloproteinases, pro-apoptotic Bax and bid, phosphatidylinositide 3-kinase/Akt1/mechanistic target of rapamycin, reactive oxygen species/apoptosis signal-regulating kinase 1/p38 mitogen-activated protein kinase, nuclear factor-κB, cluster of differentiation 1, CKD4, s6k, signal transducer and activator of transcription 3, as well as aforementioned signaling pathways . In this work, we critically review the scientific literature on the molecular targets of oleanolic acid implicated in the prevention and treatment of several types of cancer. We also discuss chemical aspects, natural sources, bioavailability, and safety of this bioactive phytochemical.

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“…OA-induced autophagy was shown for the first time in human gastric cancer cells, evidenced by the formation of GFP-RFP-LC3 puncta and autophagosomes. OA suppressed phospho-mTOR through inhibition of the PI3 K/AKT and ERK/p38 MAPK signalling pathways and through activation of the AMPK signalling pathway [21]. Hepatocellular carcinoma (HCC) is an aggressive form of cancer, with high rates of morbidity and mortality, a poor prognosis and limited therapeutic options.…”

Section: Discussionmentioning

confidence: 99%

A Triterpenoid Having Anticancer Activity Found in Stem Bark of Holoptelea integrifolia (Roxb.) Planch

Hassan¹,

Rasheed²,

Ali³

et al. 2018

Nat Prod Chem Res

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Studies on the chemical constituents of the stem bark of Holoptelea integrifolia (Roxb.) Planch have led to the isolation of a triterpenoid, oleanolic acid (1), the structure of the compound was elucidated via advanced spectroscopic techniques including EI (+), IR, 1 H-NMR and 13 C-NMR. Oleanolic acid was isolated first time from the stem bark of H. integrifolia. Crude ethylacetate extract of the stem bark of H. integrifolia has been tested in vitro for its cytotoxicity by MTT assay. This paper is based on isolation and characterization of the chemical constituents.

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Oleanolic acid induces autophagic death in human gastric cancer cells in vitro and in vivo

Cited by 34 publications

References 26 publications

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

Oleanolic Acid Alters Multiple Cell Signaling Pathways: Implication in Cancer Prevention and Therapy

A Triterpenoid Having Anticancer Activity Found in Stem Bark of Holoptelea integrifolia (Roxb.) Planch

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