Abstract

Objective: To investigate the effect of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) on lipopolysaccharide (LPS)-induced inflammatory response and oxidative stress in neonatal rat brain.Methods: Ninety-six 3-day-old Sprague Dawley rats were divided into four groups: control (saline/saline), LPS/ω-3, LPS/ω-6, and LPS/saline (n = 24/group). All rats, except those in the control group, were intraperitoneally challenged once with LPS (0.6 mg/kg) and were treated with ω-3 PUFAs, ω-6 PUFAs, or saline at 15 mL/kg for 1 or 5 consecutive days beginning on the day of LPS-challenge. Rats in the control group underwent the same procedures and received saline (vehicle). After 1 or 5 days of treatment, 12 rats from each group were sacrificed and their hippocampuses were collected. The expression of inflammation-related genes as well as the levels of oxidative stress markers in hippocampal tissues were determined.Results: After 1 or 5 days of treatment, the expression of toll-like receptor 4 and multiple proinflammatory cytokines were significantly decreased in the LPS/ω-3 group compared with those in the LPS/saline group. The activities of superoxide dismutase and glutathione (GSH) were significantly elevated, whereas amounts of malondialdehyde and oxidized glutathione (GSSG) and the ratio of GSSG/GSH were remarkably lowered in the LPS/ω-3 group compared with those in the LPS/saline group after 1 day of treatment. Opposite effects were observed in the LPS/ω-6 group.Conclusion: ω-3 PUFAs may protect rat brain tissue against LPS-induced inflammatory response and oxidative stress.

Highlights

  • Preterm birth, a leading cause of neonatal mortality, remains an important public health challenge worldwide

  • After 1 or 5 days of treatment, the expression of toll-like receptor 4 and multiple proinflammatory cytokines were significantly decreased in the LPS/ω-3 group compared with those in the LPS/saline group

  • The present study aimed to evaluate the neuroprotective effect of ω-3 polyunsaturated fatty acids (PUFAs) on LPS-induced inflammation and oxidative damage in the hippocampus of neonatal rats

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Summary

Introduction

A leading cause of neonatal mortality, remains an important public health challenge worldwide. The most common form of brain injury in premature birth survivors is white matter injury (WMI), which is defined by degeneration of preoligodendrocytes [5]. It is well-established that preoligodendrocytes are vulnerable to oxidative stress and inflammation, which are the two major mechanisms underlying the injury and death of preoligodendrocytes [3, 6]. Targeting oxidative stress and inflammation, in conjunction with antimicrobial agents, is an important adjuvant strategy that could be employed to prevent or ameliorate WMI in neonatal infections [7,8,9]

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