Picroside II Improves Severe Acute Pancreatitis-Induced Hepatocellular Injury in Rats by Affecting JAK2/STAT3 Phosphorylation Signaling.

Xuehua Piao,Baohai Liu,Tingfang Cui,Zinan Qi,Xiaodan Sui,Ying Peng

doi:10.1155/2021/9945149

Abstract

Picroside II is an important ingredient agent in Traditional Chinese medicine and hoped to reduce hepatocellular injury caused by severe acute pancreatitis (SAP). An SAP-induced hepatocellular injury model was established in rats by using pentobarbital sodium. 27 rats were divided into 3 groups: the sham group (SG), model group (MG), and Picroside groups (PG). SAP-induced hepatocellular injury was assessed using hematoxylin and eosin staining. We measured hepatocellular enzymes (amylase (AMY), alanine aminotransferase (ALT), and aspartate aminotransferase (AST)), oxidative stress factors (superoxidase dismutase (SOD) and malondialdehyde (MDA)), and inflammatory factors (tumor necrosis factor α (TNF-α), interleukin- (IL-) 6, and IL-10), apoptotic factors (BAX and cleaved caspase 3), and inflammatory signaling (Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), p-JAK2, and p-STAT3) in hepatocellular tissues. The SAP-induced hepatocellular injury model was successfully established. Picroside II treatment repaired hepatocellular injury by reducing the activities of AMY, ALT, and AST; reducing the levels of MDA, TNF-α, IL-1, IL-6, p-JAK2, p-STAT3, BAX, and cleaved caspase 3; and increasing the levels of SOD and IL-10. Picroside II exerted protective function for the SAP-induced hepatocellular injury model. Picroside II improved SAP-induced hepatocellular injury and antioxidant and anti-inflammatory properties by affecting JAK2/STAT3 phosphorylation signaling.

Highlights

Severe acute pancreatitis (SAP) is a remarkably serious illness in the pancreas, which is associated with numerous tissue failures and high risk of morbidity and mortality [1, 2]
The results suggest that Picroside II treatment increases antiapoptosis and anti-inflammatory activities by reducing relative protein levels of apoptotic factors and JAK2/STAT3 signaling in hepatocellular tissues
The model establishment affected the levels of oxidative stress biomarkers (Figure 3) and increased the levels inflammatory factors (Figure 4), apoptotic factors and inflammatory signaling JAK2/STAT3 (Figure 6), and pancreas tissue apoptosis (Figure 7)

Summary

Introduction

Severe acute pancreatitis (SAP) is a remarkably serious illness in the pancreas, which is associated with numerous tissue failures and high risk of morbidity and mortality [1, 2]. SAP development can straightforwardly induce hepatocellular injury [3, 4]. The hepatic injury cannot only worsen pancreatitis state and develop into hepatic failure and trigger mortality of SAP patients [5]. Natural products have been considered for the therapy of SPA and its induced organ failures with few side effects. Emodin, a natural anthraquinone compound isolated from the herb Rheum officinale Baill, exerts significant anti-inflammatory activities and has been found to be beneficial for the recovery of SAP by affecting via the P2X ligand-gated ion channel 7/NOD-like receptor protein 3 signaling pathway [7]. Picroside II, an active essential obtained from Picrorhiza kurrooa [8], Pseudolysimachion rotundum var. subintegrum [9], and Picrorhiza scrophulariiflora [10], is undergoing the preclinical study and exhibits

Objectives

Methods

Conclusion