ABSTRACT
The number of geriatrics with an advanced age is rising worldwide, with attendant cardiovascular disorders, characterized by elevated oxidative stress. Such oxidative stress is accelerated by an age-related loss of critical antioxidants like glutathione (GSH) and dietary solutions to combat this loss does not exist. While egg white is rich in sulphur amino acids (AAs), precursors for GSH biosynthesis, whether they can increase sulphur AA in vivo and augment GSH in the aged myocardium remain unclear. We hypothesized that egg white consumption increases GSH and reduces oxidative damage and inflammation in the geriatric heart. To this end, 101-102 week-old mice were given a AIN 76A diet supplemented with either 9% w/w egg white powder or casein for 8 weeks. Subsequent analysis revealed that egg white increased serum sulphur AA and cardiac GSH, while reducing the cysteine carrying transporter SNAT-2 and elevating glutamine transporter ASCT2 in the heart. Increased GSH was accompanied by elevated expression of GSH biosynthesis enzyme glutathione synthase as well as mitochondrial antioxidants like superoxide dismutase 2 and glutathione peroxidase 1 in egg white-fed hearts. These hearts also demonstrated lower oxidative damage of lipids (4-hydroxynonenal) and proteins [nitrotyrosine] with elevated anti-inflammatory IL-10 gene expression. These data demonstrate that even at the end of lifespan, egg whites remain effective in promoting serum sulphur AAs and preserve cardiac GSH with potent anti-oxidant and mild anti-inflammatory effects in the geriatric myocardium. We conclude that egg white intake may be an effective dietary strategy to attenuate oxidative damage in the senescent heart.
Subject(s)
Aging , Animal Feed , Egg White/chemistry , Glutathione/metabolism , Myocardium/pathology , Oxidative Stress , Aldehydes/pharmacology , Amino Acids, Sulfur/metabolism , Animals , Antioxidants/metabolism , Glutathione Synthase/metabolism , Inflammation , Lipid Peroxidation , Male , Mice , Mice, Inbred C57BL , Myocardium/metabolism , Tyrosine/analogs & derivatives , Tyrosine/pharmacologyABSTRACT
Objective To explore the effect of low-frequency electroacupuncture (EA) on neuropathic pain induced by spinal nerve injury and its underlying mechanism.Methods Thirty-two male Sprague-Dawley rats were randomly divided into a normal group,a sham spared nerve injury (SNI) group,an SNI group and an SNI+EA group,each of 8.The rats in the SNI and SNI+EA groups were given SNI surgery,while those of the sham-SNI group only had the sciatic nerve and its branches exposed without any lesion.EA at 2 Hz was applied over the ipsilateral Zusanli and Kunlun acupoints daily for 14 days after the surgery.The ipsilateral paw withdrawal threshold (PWT) was measured,along with protein kinase A (PKA) levels in the dorsal horn of the spinal cord,calcitonin gene-related peptide (CGRP) and substance P (SP) levels along with transient receptor potential V1 (TRPV1).Results Compared to the normal group,the SNI groups all showed significant decreases in their PWTs on the affected side and significant increases in PKA,TRPV1,CGRP and substance P on the affected side.Compared to SNI group,the average ipsilateral PWT in the SNI+EA group increased significantly after EA treatment,while PKA levels,TRPV1,CGRP levels and SP expression all decreased significantly.Conclusion Electroacupuncture at low frequency can effectively relieve neuropathic pain,perhaps through down-regulation of PKA in the spinal cord and by decreasing pain hypersensitivity related to CGRP and SP.
