Abstract

Liver regeneration is the basic physiological process after partial hepatectomy (PH), and is important for the functional rehabilitation of the liver after acute hepatic injury. This study was designed to explore the effects of neurolytic celiac plexus block (NCPB) on liver regeneration after PH. We established a model of PH in rats, assessing hepatic blood flow, liver function, and serum CRP, TNF-α, IL-1β and IL-6 concentrations of the residuary liver after PH. Additionally, histopathological studies, immunohistochemistry, and western blotting were also performed. Our results indicated that NCPB treatment after PH improved liver regeneration and survival rates, increased hepatic blood flow, reduced hepatocyte damage, decreased the secretion and release of inflammatory cytokines, increased the expression of B cell lymphoma/leukemia-2 (Bcl-2), and decreased the expression of Bcl-2 associated X protein (Bax). Additionally, Western blotting revealed that the expression of NF-κB p65 and c-Jun were decreased in liver after NCPB. In conclusion, the results of our present study indicate that NCPB treatment has a favorable effect on liver regeneration after PH. We suggest that NCPB can be utilized as an effective therapeutic method to help the functional rehabilitation of the liver after acute hepatic injury or liver cancer surgery.

Highlights

  • The liver is the largest intra-abdominal organ for maintaining vital movement, and there is currently no way to compensate for the absence of liver function long term

  • The weight of liver was obviously increased at 3 and 7 days after partial hepatectomy (PH) (p,0.05); in addition, the liver weight of neurolytic celiac plexus block (NCPB) group was significantly higher than that of control group (p,0.05). This result indicated that NCPB treatment can significantly improve the liver regeneration of rats after PH

  • The current study demonstrates that NCPB has a potent protective effect against mortality in rats following PH; we discuss the results of experiments designed to understand the mechanisms underlying this effect

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Summary

Introduction

The liver is the largest intra-abdominal organ for maintaining vital movement, and there is currently no way to compensate for the absence of liver function long term. After severe liver injury or surgical resection, liver cells must regenerate to compensate for the lost tissue. Due to the injury, pain, blood loss, shock, acidosis and other stimuli after severe injury or hepatic cancer surgery, intense stress and inflammatory responses can be induced, causing obvious stress disorder [2]. It has been reported that post-traumatic stress disorder is an important and key initiating factor of secondary injury to the body, including systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome [3]. T lymphocyte-mediated immune function is significantly inhibited, so the body’s capacity for defending against infection is lower, leading to an increased susceptibility to infection and multiple organ failure [4]. Mechanisms to promote liver tissue regeneration and inhibit the development of SIRS are important for decreasing mortality after sever liver injury or liver cancer surgery

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