Oleanolic Acid Induces Apoptosis and Necrosis in Lo2 Cells

Xiao, Qingwen; Yuanfu, LU; Chen, Xiuping

doi:10.36468/pharmaceutical-sciences.657

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…After 72 h, highest percentage of necrotic cells could be seen in the treatment of higher concentrations of both compounds. This outcome is similar to those reported in other forms of cell lines [ 25 , 26 ], suggesting that cells that are not acutely damaged may activate a programmed suicide mechanism while acute cytotoxicity may cause necrosis.…”

Section: Discussionsupporting

confidence: 87%

Anticancer Potential of Damnacanthal and Nordamnacanthal from Morinda elliptica Roots on T-lymphoblastic Leukemia Cells

et al. 2021

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Background: This study reports on the cytotoxic properties of nordamnacanthal and damnacanthal, isolated from roots of Morinda elliptica on T-lymphoblastic leukaemia (CEM-SS) cell lines. Methods: MTT assay, DNA fragmentation, ELISA and cell cycle analysis were carried out. Results: Nordamnacanthal and damnacanthal at IC50 values of 1.7 μg/mL and10 μg/mL, respectively. At the molecular level, these compounds caused internucleosomal DNA cleavage producing multiple 180–200 bp fragments that are visible as a “ladder” on the agarose gel. This was due to the activation of the Mg2+/Ca2+-dependent endonuclease. The induction of apoptosis by nordamnacanthal was different from the one induced by damnacanthal, in a way that it occurs independently of ongoing transcription process. Nevertheless, in both cases, the process of dephosphorylation of protein phosphates 1 and 2A, the ongoing protein synthesis and the elevations of the cytosolic Ca2+ concentration were not needed for apoptosis to take place. Nordamnacanthal was found to have a cytotoxic effect by inducing apoptosis, while damnacanthal caused arrest at the G0/G1 phase of the cell cycle. Conclusion: Damnacanthal and nordamnacanthal have anticancer properties, and could act as potential treatment for T-lymphoblastic leukemia.

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Section: Discussionsupporting

confidence: 87%

Anticancer Potential of Damnacanthal and Nordamnacanthal from Morinda elliptica Roots on T-lymphoblastic Leukemia Cells

et al. 2021

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“…However, clinical use of OA‐containing herbal medicines can cause cholestatic liver injury (Milkiewicz & Heathcote, 2011). Studies have found that high concentrations of OA can cause cytotoxic effects (Tuncay et al, 2018; Xiao et al, 2020), while in animal experimental studies show that OA can cause cholestatic liver injury (Liu, 2005; Sato et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

AMP‐activated protein kinase‐farnesoid X receptor pathway contributes to oleanolic acid‐induced liver injury

Huang

Liao

et al. 2023

J of Applied Toxicology

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Natural pentacyclic triterpenoid oleanolic acid (OA) is used as an over-the-counter drug for acute and chronic hepatitis. However, clinical use of OA-containing herbal medicines has been reported to cause cholestasis, and the specific mechanism is unknown. The purpose of this study was to explore how OA causes cholestatic liver injury via the AMP-activated protein kinase (AMPK)-farnesoid X receptor (FXR) pathway. In animal experiments, it was found that OA treatment activated AMPK and decreased FXR and bile acid efflux transport proteins expression. When intervened with the specific inhibitor Compound C (CC), it was observed that AMPK activation was inhibited, the reduction of FXR and bile acid efflux transport protein expression was effectively alleviated, serum biochemical indicators were significantly reduced, and liver pathological damage brought about by OA was effectively ameliorated. In addition, OA was found to downregulate the expression of FXR and bile acid efflux transport proteins by activating the ERK1/2-LKB1-AMPK pathway in cellular experiments. The ERK1/2 inhibitor U0126 was used to pretreat primary hepatocytes, and this drastically reduced the phosphorylation levels of LKB1 and AMPK. The inhibition effects of OA on FXR and bile acid efflux transport proteins were also effectively alleviated after pretreatment with CC. In addition, OA-induced downregulation of FXR gene and protein expression levels was significantly prevented after silencing AMPKα1 expression in AML12 cells. Our study demonstrated that OA inhibited FXR and bile acid efflux transporters through the activation of AMPK, thus leading to cholestatic liver injury.

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Suppression of SIRT1/FXR signaling pathway contributes to oleanolic acid-induced liver injury

Liao

Huang

et al. 2023

Toxicology and Applied Pharmacology

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Oleanolic Acid Induces Apoptosis and Necrosis in Lo2 Cells

Cited by 4 publications

References 28 publications

Anticancer Potential of Damnacanthal and Nordamnacanthal from Morinda elliptica Roots on T-lymphoblastic Leukemia Cells

Anticancer Potential of Damnacanthal and Nordamnacanthal from Morinda elliptica Roots on T-lymphoblastic Leukemia Cells

AMP‐activated protein kinase‐farnesoid X receptor pathway contributes to oleanolic acid‐induced liver injury

Suppression of SIRT1/FXR signaling pathway contributes to oleanolic acid-induced liver injury

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