Role of hepatic stellate cells in fibrogenesis in a model of pomegranate-treated fatty liver induced by junk food in male albino rats immunohistochemical and electron microscopic study

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Abstract

Introduction

Hepatic fibrogenesis is a common result of liver injury. It is believed to be a critical factor that leads to hepatic failure. A critical event in fibrogenesis is activation of hepatic stellate cells (HSCs).

Aim of work

The aim of this investigation was to study the role of HSCs in fibrogenesis in a model of pomegranate juice (PJ)-treated fatty liver induced by junk food using immunohistochemical and electron microscopic study.

Materials and methods

Thirty young male albino rats were divided into control (I) and experimental (II) groups. Group II was further divided into two subgroups: II-a (junk food) and II-b (pomegranate juice + junk food). After 8 weeks, blood samples were collected for detection of leptin and tumour necrosis factor alpha TNF-α.Then half of the liver samples were processed for light microscopic examination, whereas the other half were prepared for electron microscopic examination. Paraffin sections were stained using H&E, glial ibrillary acid protein, α-smooth muscle actin, TNF-α, and transforming growth factor -beta-1 TGF-β1. Morphometric and statistical studies for assessing immunoexpression were carried out.

Results

HSC's markers glial fibrilar acid protein and α-smooth muscle actin and cytokines TNF-α and TGF-β1 in subgroup II-a showed strong positive immunoexpression. Electron microscopic study showed activated - HSCs containing granules and collagen fibrils. Proliferative and myofibroblast -HSCs were also seen in the same group. Subgroup II-b showed a nonsignificant increase in immunoexpression of HSC's markers and cytokines. However, only activated- HSCs were seen.

Conclusion and recommendation

Immunoexpression of HSC markers and cytokines may be used as an indicator for liver fibrosis. Presence of different types of HSCs in fatty liver explains their role in fibrosis. Further experimental and clinical studies directed toward inhibiting the activity of HSC may delay or prevent liver fibrosis occurs in many pathological conditions.

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