Related Experiment Video

Updated: Feb 5, 2026

Early Detection of Drug-Induced Renal Hemodynamic Dysfunction Using Sonographic Technology in Rats
06:38

Early Detection of Drug-Induced Renal Hemodynamic Dysfunction Using Sonographic Technology in Rats

Published on: March 11, 2016

12.6K

Acute renal injury induced by endotoxic shock in rats is alleviated via PI3K/Nrf2 pathway

C-H Chuang1, C-K Yang, P-H Wu

  • 1Department of Emergency Medicine, Xiamen Changgung Hospital, Medical College of Xiamen University Teaching Hospital, Xiamen. flystar@gmail.com.

European Review for Medical and Pharmacological Sciences
|September 5, 2018
PubMed
Abstract

Insights

Acute kidney injury (AKI) in rats from endotoxic shock is regulated by the PI3K/Nrf2 pathway. Heme oxygenase 1 (HO-1) appears crucial in protecting against AKI.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathophysiology

Background:

  • Acute kidney injury (AKI) is a critical complication of endotoxic shock.
  • The PI3K/Nrf2 signaling pathway's role in AKI pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the involvement of the PI3K/Nrf2 pathway in endotoxic shock-induced AKI in a rat model.
  • To assess the protective potential of modulating this pathway.

Main Methods:

  • Constructed an endotoxic shock rat model with three groups: control, endotoxic shock, and wortmannin + endotoxic shock.
  • Evaluated renal tissue pathology using histological scores (HSK).
  • Measured biochemical markers (BUN, Cr, α1-MG), enzyme activities (SOD, MDA), and protein/mRNA expression (Akt, Nrf2, HO-1) via Western blot and qRT-PCR.

Main Results:

  • Endotoxic shock significantly increased HSK, BUN, Cr, α1-MG, and MDA, while decreasing SOD activity compared to controls.
  • Wortmannin treatment exacerbated these pathological and biochemical changes.
  • Expression of Nrf2, HO-1, and Akt (phosphorylated) was altered in the wortmannin-treated group, indicating pathway modulation.

Conclusions:

  • The PI3K/Nrf2 pathway plays a significant role in regulating AKI induced by endotoxic shock in rats.
  • Heme oxygenase 1 (HO-1) emerges as a key effector protein with potential protective functions against AKI in this context.

More Related Videos

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

950
A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion09:02

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion

Published on: February 2, 2021

4.9K

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.6K
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
756
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
1.1K
Acute Kidney Injury VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

Acute Kidney Injury (AKI) results in an inability to maintain fluid, electrolyte, and acid-base balance. Effective nursing management is critical in improving patient outcomes and includes comprehensive patient assessment and targeted interventions.Comprehensive Patient AssessmentA detailed history collection is essential, focusing on any recent infections, nephrotoxic medication use, or chronic conditions such as hypertension and diabetes that may contribute to AKI. During the physical...
481
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

Acute Kidney Injury (AKI) requires a collaborative healthcare approach to restore renal function and prevent complications. Essential management strategies involve monitoring fluid and electrolyte balance, adjusting medications, initiating dialysis when necessary, and providing nutritional support.Fluid and Electrolyte ManagementFluid Monitoring: Regularly monitoring body weight, central venous pressure, and urine output helps detect fluid imbalances early. Patient intake and output are...
362
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
950