Effect of remained stem height on yield, quality of Inula helenium I. and on soil water content

Ma, Lingfa; He, Shun; Li, Fenrui; Yang, Jin; Chang, Yu‐Wei; Zhao, Kaihui; Liu, Ningyu

doi:10.1016/j.sjbs.2017.10.016

Cited by 5 publications

(5 citation statements)

References 6 publications

(3 reference statements)

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“…Alantolactone (AL), one of the significant sesquiterpene lactone compounds, is isolated from the root of Inula Helenium L and has a variety of biological activities, such as anti-inflammatory, antimicrobial, and especially anticancer activities. , AL can inhibit the activity of TrxR1, increase the level of ROS in cancer cells, and oxidatively damage cancer cells, which may reverse the reduction and detoxification mechanisms of Pt-based chemotherapeutics. − Meanwhile, AL can induce mitochondrial membrane potential (Δψ m ) depolarization and mitochondrial dysfunction by inhibiting the activity of TrxR1 to increase the level of ROS, which reactivates the mitochondrial apoptotic pathway and potentially reverses the apoptosis-blocking mechanism. , However, AL is unstable due to its rapid metabolism, limited solubility, and low bioavailability, which limit its further development in clinical applications.…”

Section: Introductionmentioning

confidence: 99%

Alantolactone-Loaded Pegylated Prodrug Nanocarriers for Synergistic Treatment of Cisplatin-Resistant Ovarian Cancer via Reactivating Mitochondrial Apoptotic Pathway

Luo

Liang

et al. 2022

ACS Biomater. Sci. Eng.

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Ovarian cancer (OV) seriously damages women’s health because of refractory OV and the development of platinum (Pt) resistance. New treatment strategies are urgently needed to deal with the treatment of cisplatin-resistant OV. Here, a reduction-sensitive pegylated Pt(IV) prodrug was synthesized by amidation of methoxy polyethylene glycol amine (PEG750-NH2) with monocarboxylic Pt(IV) prodrug (Pt(IV)-COOH). Then alantolactone (AL) loaded PEG-Pt(IV) nanocarriers (NP(Pt)@AL) were prepared. In the cisplatin-resistant model of OV, cancer cells actively ingest NP(Pt)@AL through endocytosis, and AL and Pt(II) were disintegrated and released under high intracellular reductant condition. The activity of thioredoxin reductase 1 (TrxR1) inhibited by AL and the adducts of Pt(II) with mitochondrial DNA (mDNA) can costimulate reactive oxygen species (ROS) and reactivate the mitochondrial pathway of apoptosis. Meanwhile, Pt(II) binds with nuclear DNA (nDNA) to jointly promote cell apoptosis. Both in vitro and in vivo results demonstrated that NP(Pt)@AL could effectively reverse the drug resistance and displayed excellent synergistic therapeutic efficacy on platinum-resistant OV with high safety. Therefore, reactivation of the mitochondrial pathway of apoptosis would be a potential strategy to improve the therapeutic effect of Pt-based chemotherapy and even reverse drug resistance.

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Section: Introductionmentioning

confidence: 99%

Alantolactone-Loaded Pegylated Prodrug Nanocarriers for Synergistic Treatment of Cisplatin-Resistant Ovarian Cancer via Reactivating Mitochondrial Apoptotic Pathway

Luo

Liang

et al. 2022

ACS Biomater. Sci. Eng.

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“…ALT, a major bioactive sesquiterpene component of Inula helenium, has been reported to possess multiple biological and pharmacological properties including antibacterial, antifungal, anti-in ammatory and anticancer effects [7]. In recent years, ALT has been reported to exert anti-tumor effects in several types of cancer, including lung cancer, gastric cancer, hepatic cancer, B-cell acute lymphoblastic leukemia, pancreatic cancer and breast cancer [8].…”

Section: Introductionmentioning

confidence: 99%

Alantolactone inhibits cell autophagy and promotes apoptosis via AP2M1 in acute lymphoblastic leukemia

Shi

Lan

Wang

et al. 2020

Preprint

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Background: Acute lymphoblastic leukemia (ALL) is an aggressive hematopoietic malignancy that is most commonly observed in children. Alantolactone (ALT) has been reported to exhibit anti-tumor activity in different types of cancer. The aim of the present study was to investigate the anti-tumor activity and molecular mechanism of ALT in ALL. Methods: ALL cell lines were treated with 1, 5 and 10 μM ALT, and cell viability was assessed using an MTT assay and RNA sequencing. Flow cytometry, JC-1 staining and immunofluorescence staining assays were used to measure cell apoptosis and autophagy. Additionally, western blot analysis was used to detect expression of apoptosis and autophagy related proteins. Finally, the effects of ALT on tumor growth were assessed in a BV173 xenograft nude mouse model. Results: ALT inhibited the proliferation of ALL cells in a dose-dependent manner. Additionally, it was demonstrated that ALT inhibited cell proliferation, colony formation, autophagy, induced apoptosis and reduced tumor growth in vivo through upregulating the expression of adaptor related protein complex 2 subunit mu 1 (AP2M1). Moreover, the autophagy activator rapamycin, attenuated the pro-apoptotic effects of ALT on BV173 and NALM6 cell lines. Overexpression of AP2M1 decreased the expression of Beclin1 and the LC3-II/LC3-1 ratio, and increased p62 expression. Knockdown of Beclin1 increased the levels of bax, cleaved caspase 3 and cytochrome C, and decreased bcl-2 expression. Conclusions: The present study demonstrated that ALT exerts anti-tumor activity through inducing apoptosis and inhibiting autophagy by upregulating AP2M1 in ALL, highlighting a potential therapeutic strategy for treatment of ALL.

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“…ALT, a major bioactive sesquiterpene component of Inula helenium, has been reported to possess multiple biological and pharmacological activities including antibacterial, antifungal, antiin ammatory and anticancer effects [7]. In recent years, ALT has been reported to exert antitumor effect on many cancers, including lung cancer, gastric cancer, hepatic cancer, B-cell acute lymphoblastic leukemia, pancreatic cancer and breast cancer [8].…”

Section: Introductionmentioning

confidence: 99%

Alantolactone inhibits cell autophagy and promotes apoptosis through targeting AP2M1 in acute lymphotic leukemia

Shi¹,

Wang²,

Yang³

et al. 2020

Preprint

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Abstract Background: Acute lymphoblastic leukemia (ALL) is an aggressive hematopoietic malignancy that is most common in children. Alantolactone (ALT) has been reported to have antitumor activity in different types of cancers. This study aimed to investigate the antitumor activity and molecular mechanism of ALT in ALL. Methods: The ALL cell lines were treated with 1, 5 and 10μM of ALT, and then subjected to MTT assay and RNA sequencing. Flow cytometry, JC-1 staining and immunofluorescence staining assays were employed to measure cell apoptosis and autophagy. Meanwhile, Western blot analysis was used to detect apoptosis and autophagy related proteins. Finally, the effect of ALT on tumor growth was measured in BV173 xenograft nude mouse model. Results: In this study, we demonstrated that ALT inhibited the proliferation of ALL cells in does-dependent manner. A series of experiments demonstrated that ALT inhibited cell proliferation, colony formation, autophagy, induced apoptosis and restained tumor growth in vivo through upregulating adaptor related protein complex 2 subunit mu 1 (AP2M1). Moreover, autophagy activator rapamycin attenuated the pro-apoptotic effect of ALT on BV173 and NALM6 cell lines. Further, overexpressed AP2M1 decreased the expression of Beclin1, LC3-II/LC3-1 ratio and increased p62 expression. Fianally, knockdown of Beclin1 increased the levels of bax, cleaved caspase 3 and cytochrome C and decreased bcl-2 expression. Conclusions: This study demonstrated that ALT exerts antitumor activity through inducing apoptosis and inhibiting autophagy by upregulating AP2M1 in ALL, indicating a potential therapeutic strategy for ALL treatment.

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Effect of remained stem height on yield, quality of Inula helenium I. and on soil water content

Cited by 5 publications

References 6 publications

Alantolactone-Loaded Pegylated Prodrug Nanocarriers for Synergistic Treatment of Cisplatin-Resistant Ovarian Cancer via Reactivating Mitochondrial Apoptotic Pathway

Alantolactone-Loaded Pegylated Prodrug Nanocarriers for Synergistic Treatment of Cisplatin-Resistant Ovarian Cancer via Reactivating Mitochondrial Apoptotic Pathway

Alantolactone inhibits cell autophagy and promotes apoptosis via AP2M1 in acute lymphoblastic leukemia

Alantolactone inhibits cell autophagy and promotes apoptosis through targeting AP2M1 in acute lymphotic leukemia

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