Coenzyme Q10 Ameliorates Pancreatic Fibrosis via the ROS-Triggered mTOR Signaling Pathway

المؤلفون المشاركون

Xue, Ran
Gao, Yan
Pang, Yanhua
Hao, Jianyu
Wang, Jianxin
Yang, Lixin
Liu, Xinjuan
Wang, Yanbin

المصدر

Oxidative Medicine and Cellular Longevity

العدد

المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-10، 10ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2019-02-07

دولة النشر

مصر

عدد الصفحات

10

التخصصات الرئيسية

الأحياء

الملخص EN

Aim.

Pancreatic stellate cells (PSCs) play a pivotal role in pancreatic fibrosis.

Any remedies that inhibit the activation of PSCs can be potential candidates for therapeutic strategies in pancreatic fibrosis-related pancreatic ductal adenocarcinoma (PDAC) and chronic pancreatitis (CP).

Our study is aimed at exploring the protective effect of coenzyme Q10 (CoQ10) against pancreatic fibrosis.

Methods.

Pancreatic fibrosis was induced by 20% L-arginine (250 mg/100 g) at 1 h intervals twice per week for 8 weeks in C57BL/6 mice.

CoQ10 was administered for 4 weeks.

Isolated primary PSCs from C57BL/6 mice were treated with 100 μM CoQ10 for 72 h, as well as Rosup and specific inhibitors.

The effects of CoQ10 on the activation of PSCs, autophagy, collagen deposition, histological changes, and oxidative stress were analyzed by western blotting, biochemical estimations, immunofluorescence staining, and hematoxylin-eosin, Masson, and Sirius red staining, as well as with a reactive oxygen species (ROS) assay.

Results.

Pretreatment and posttreatment of CoQ10 decreased autophagy, activation of PSCs, oxidative stress, histological changes, and collagen deposition in the CP mouse model.

In primary PSCs, expression levels of p-PI3K, p-AKT, and p-mTOR were upregulated with CoQ10.

A rescue experiment using specific inhibitors of the PI3K-AKT-mTOR pathway demonstrated that the PI3K-AKT-mTOR signaling pathway was the underlying mechanism by which CoQ10 ameliorated fibrosis.

With the addition of Rosup, expression levels of the autophagy biomarkers LC3 and Atg5 were elevated.

Meanwhile, the levels of p-PI3K, p-AKT, and p-mTOR were lower.

Conclusions.

Our findings demonstrated that CoQ10 alleviates pancreatic fibrosis by the ROS-triggered PI3K/AKT/mTOR signaling pathway.

CoQ10 may be a therapeutic candidate for antifibrotic methods.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Xue, Ran& Wang, Jianxin& Yang, Lixin& Liu, Xinjuan& Gao, Yan& Pang, Yanhua…[et al.]. 2019. Coenzyme Q10 Ameliorates Pancreatic Fibrosis via the ROS-Triggered mTOR Signaling Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1205416

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Xue, Ran…[et al.]. Coenzyme Q10 Ameliorates Pancreatic Fibrosis via the ROS-Triggered mTOR Signaling Pathway. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-10.
https://search.emarefa.net/detail/BIM-1205416

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Xue, Ran& Wang, Jianxin& Yang, Lixin& Liu, Xinjuan& Gao, Yan& Pang, Yanhua…[et al.]. Coenzyme Q10 Ameliorates Pancreatic Fibrosis via the ROS-Triggered mTOR Signaling Pathway. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1205416

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1205416