Abstract

Vitamin B6 (VitB6) is a water-soluble vitamin and includes pyridoxine, pyridoxal, pyridoxamine, and their phosphorylated forms. In the current study, we demonstrated that VitB6 could improve lipopolysaccharide (LPS)–induced myocardial injury. We demonstrated that VitB6 can suppress LPS-induced oxidative stress and lipid peroxidation that lead to ferroptosis and apoptosis in vivo and in vitro. Moreover, we found that VitB6 can regulate the expression of iron regulatory proteins, maintaining intracellular iron homeostasis. To confirm that VitB6 could inhibit LPS-induced ferroptosis and apoptosis, we pretreated mice with ferrostatin-1 (Fer-1) and emricasan that efficiently mimicked VitB6 pharmacological effects. This improved the survival rate of mice challenged with a high LPS dose. In addition, VitB6 regulated the expression of LPS-induced apoptosis-related proteins and iron regulatory proteins. It mediated the expression of Nrf2, transcription factor NF-E2–related factor 2, which promoted the expression of antioxidant enzymes and restrained LPS-induced ferroptosis and apoptosis. Overall, our results indicated that VitB6 can be used on novel therapies to relieve LPS-induced myocardial injury.

Highlights

  • Vitamin B6 (VitB6), such as pyridoxine, pyridoxal, pyridoxamine, and pyridoxal 5′-phosphate (PLP), is a pivotal cofactor of more than 100 enzymes (Benabdellah et al, 2009)

  • The ejection fraction (EF) and fractional shortening (FS) significantly decreased in LPS group mice compared with controls, but cardiac dysfunction improved in the VitB6+LPS group (Figures 1A–C)

  • We demonstrated that VitB6 improved LPS-induced myocardial dysfunction

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Summary

Introduction

Vitamin B6 (VitB6), such as pyridoxine, pyridoxal, pyridoxamine, and pyridoxal 5′-phosphate (PLP) (the biologically active form of VitB6), is a pivotal cofactor of more than 100 enzymes (Benabdellah et al, 2009). VitB6 is important in the deamination and transamination of amino acids, gluconeogenic metabolism, ornithine cycle, and heme biosynthesis (Benabdellah et al, 2009). Heme synthesis will be blocked when VitB6 is deficient or depleted, resulting in lowpigment small-cell anemia and iron elevation (Yasuda et al, 2015). It has been indicated that VitB6 can prevent lipid peroxidation and oxygen radical production, induced by hydrogen peroxide (Kannan and Jain, 2004; Molina-López et al, 2016). VitB6 could prevent oxidative stress caused by homocysteine (Hsu et al, 2015).

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