Detoxification strategies of triptolide based on drug combinations and targeted delivery methods

Cao, Zhiwen; Liu, Bin; Li, Li; Lu, Peipei; Lan, Yan; Lü, Cheng

doi:10.1016/j.tox.2022.153134

Cited by 8 publications

(4 citation statements)

References 112 publications

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“…Previous animal studies have shown that crocin is a protective against doxorubicin-induced nephrotoxicity and cyclophosphamide-induced hepatotoxicity through modulation of antioxidant enzymes and inflammatory mediators ( Jnaneshwari et al, 2013 ; Hussain et al, 2021 ). Combined treatment with vitamin C and TP could combat oxidative stress by regulating the levels of SOD, GSH, CAT and MD ( Xu et al, 2019 ), which agrees with the known mechanisms for TP-induced hepatotoxicity ( Cao et al, 2022 ). TP may lead to emergency oxidative damage of liver cells by reducing thioredoxin activity ( Shen et al, 2019 ).…”

Section: Discussionsupporting

confidence: 71%

The Effect of Triptolide Combined With Crocin on Arthritis in Mice: From Side Effect Attenuation to Therapy

Yan

Zhang

et al. 2022

Front. Pharmacol.

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Clinical use of triptolide (TP) is restricted due to severe toxicity. This study assessed the protective effect of crocin (CR) as a natural antioxidant against TP-induced toxicity in bovine collagen type II-induced arthritis (CIA) in mice. The mice in the CIA model group showed macroscopic signs of severe arthritis. The anti-arthritis effects in the control, TP + CR, and TP groups were evaluated through assessment of foot volume, arthritis score, and proinflammatory cytokines, and collagen antibody assay. Crocin reduced TP-induced toxicity, as evidenced by evaluation of survival rate, body weight, visceral index, hepatic and renal functions, histopathologic analyses, and antioxidant enzyme activities. Transcriptome sequencing resulted in identification of 76 differentially expressed genes (DEGs) associated with hepatotoxicity between the TP and TP + CR groups. Of these, Three DEGs (Cyp1a2,Gsta4, and Gstp1) were validated using quantitative real-time PCR analysis. In conclusion, CR protected CIA mice from TP-induced toxicity through modulation of the cytochrome P450 and glutathione metabolism pathways.

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Section: Discussionsupporting

confidence: 71%

The Effect of Triptolide Combined With Crocin on Arthritis in Mice: From Side Effect Attenuation to Therapy

Yan

Zhang

et al. 2022

Front. Pharmacol.

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“…However, by combination therapy of triptolide with quercitin, its toxic effects on liver can be reversed by regulating Treg/Th17 balance. Later, studies conducted on quercitin has revealed its impact on hepatitis induced by triptolide via Treg/Th17 balance modulation through TIM-3 pathway [ 65 ].…”

Section: Pharmacological Effects Of Triptolide Against Various Tumorsmentioning

confidence: 99%

Mechanisms of cancer cell death induction by triptolide: A comprehensive overview

Feng,

Li,

Bai

et al. 2024

Heliyon

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“…Small interfering RNA targeting ribosomal protein L4 (siRPL4) exaggerates the inhibitory effects of triptolide on RPL4 protein In subsequent experiments, the toxicity of the transfection reagent slightly damaged the cells during transfection; moreover, TP was also toxic to a certain extent (Cao et al, 2022). Therefore, we empirically reduced the dose of TP to 25 ng/mL for A549 cells and 6.5 ng/mL for PC9 cells to ensure good cell viability.…”

Section: Triptolide Inhibits Ribosomal Protein L4 Mrna and Protein Ex...mentioning

confidence: 99%

Silencing ribosomal protein L4 enhances the inhibitory effects of triptolide on non-small cell lung cancer cells by disrupting the mouse double minute 2 protein–P53 tumor suppressor pathway

TANG,

ZHAN,

MAO

et al. 2023

Biocell

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Non-small cell lung cancer (NSCLC) is a malignant tumor with high incidence worldwide. Triptolide (TP), extracted from Tripterygium wilfordii Hook F, exhibits potent broad-spectrum antitumor activity. Although some mechanisms through which TP inhibits NSCLC are well understood, those that involve ribosomal proteins remain yet to be understood. In this study, the transcriptome and proteome were integrated and analyzed. Our data indicated ribosomal protein L4 (RPL4) to be a core hub protein in the protein-protein interaction network. RPL4 is overexpressed in NSCLC tissues and cells. Transfection with siRPL4 or TP treatment alone arrested the cell cycle in the G1 phase, induced cell apoptosis, and repressed cell invasion. Compared to treating cells with TP alone or siRPL4, treating them with siRPL4-TP enhanced the inhibition of NSCLC cells. Reduced RPL4 expression reinforced the inhibitory effects of TP on NSCLC cells by disrupting the MDM2-P53 pathway and by altering the expression of PARP1/Snail/cyclin D1. In vivo assays verified that TP induced cell apoptosis and reduced RPL4 expression in xenografts. These findings provide clues to facilitate the development of effective TP-based therapeutic strategies to kill NSCLC cells.

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Detoxification strategies of triptolide based on drug combinations and targeted delivery methods

Cited by 8 publications

References 112 publications

The Effect of Triptolide Combined With Crocin on Arthritis in Mice: From Side Effect Attenuation to Therapy

The Effect of Triptolide Combined With Crocin on Arthritis in Mice: From Side Effect Attenuation to Therapy

Mechanisms of cancer cell death induction by triptolide: A comprehensive overview

Silencing ribosomal protein L4 enhances the inhibitory effects of triptolide on non-small cell lung cancer cells by disrupting the mouse double minute 2 protein–P53 tumor suppressor pathway

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