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一种基于藏红花的多草药配方DuK可预防雄性Wistar大鼠的肝细胞癌。

A Saffron-based Polyherbal Formulation DuK Prevents Hepatocellular Carcinoma in Male Wistar Rats.

作者信息

Gupta Meenakshi, Nimesh Hemlata, Bilgrami Anwar L, Sarwat Maryam

机构信息

Amity Institute of Pharmacy, Amity University, Noida, Uttar Pradesh, India.

Deanship of Scientific Research, King Abdulaziz University, Jeddah, Saudi Arabia.

出版信息

Curr Cancer Drug Targets. 2025;25(4):335-344. doi: 10.2174/1568009623666230818115905.

Abstract

BACKGROUND

Duk is a well-established traditional drug that has been used since time immemorial by Indian practitioners to cure various human ailments.

OBJECTIVE

The purpose of this study was to explore the anti-cancer activity and the possible mechanism of Duk against diethylnitrosamine (DEN)-initiated hepatocarcinogenesis.

METHODS

We administered Duk at 3 doses, viz., 75, 150, and 300 mg/kg/day, 2 weeks before the DEN and continued it for 16 weeks. After 1 week of DEN recovery, 2-aminoacetylflourine (2- AAF) was administered to promote hepatocarcinogenesis.

RESULTS

We found that Duk significantly reduced the DEN and 2-AAF induced phenotypical changes in rats and restored the levels of liver function markers. Furthermore, Duk counteracted the oxidative stress induced by carcinogens as observed by restoration in the levels of superoxide dismutase (SOD) and catalase (CAT). Duk significantly diminished the levels of malondialdehyde (MDA) in a dose dependent manner and restored the liver microarchitecture as assessed by histopathological studies. The results of immunohistochemical staining showed that Duk inhibited the DEN-induced decrease in the number of cells positive for Bid and Caspase-9. It also reduces the number of cells positive for Cyclin D.

CONCLUSION

Duk significantly protects rat liver from hepatocarcinogenesis by regulating oxidative damage and restoring liver function markers. The chemopreventive effect of Duk might be through the induction of apoptosis.

摘要

背景

Duk是一种历史悠久的传统药物,印度从业者自古以来就用它来治疗各种人类疾病。

目的

本研究旨在探讨Duk对二乙基亚硝胺(DEN)引发的肝癌发生的抗癌活性及可能机制。

方法

在给予DEN前2周,我们以3种剂量,即75、150和300mg/kg/天给予Duk,并持续给药16周。在DEN恢复1周后,给予2-氨基乙酰氟(2-AAF)以促进肝癌发生。

结果

我们发现Duk显著减少了DEN和2-AAF诱导的大鼠表型变化,并恢复了肝功能标志物水平。此外,如超氧化物歧化酶(SOD)和过氧化氢酶(CAT)水平的恢复所示,Duk抵消了致癌物诱导的氧化应激。Duk以剂量依赖方式显著降低丙二醛(MDA)水平,并通过组织病理学研究评估恢复了肝脏微结构。免疫组织化学染色结果显示,Duk抑制了DEN诱导的Bid和Caspase-9阳性细胞数量的减少。它还减少了细胞周期蛋白D阳性细胞的数量。

结论

Duk通过调节氧化损伤和恢复肝功能标志物,显著保护大鼠肝脏免受肝癌发生。Duk的化学预防作用可能是通过诱导细胞凋亡实现的。

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