Abstract:
BACKGROUND : It has been said that there is a probable “head-to-heart” link in resulting in the development of Alzheimer’s disease (AD). This is because cardiovascular (CV) and neurodegenerative diseases such as AD share many risk factors. Researchers have theorised that a significant contributor to the neurological and CV complications in AD may be due to exposure to the lipopolysaccharide (LPS) endotoxin that results in a low-grade systemic inflammatory immune response. Systemic inflammation impacts both the CV and neurological systems in harmful ways. The elderly is more vulnerable to exposure since they are increasingly likely to suffer from tooth loss or gastrointestinal tract impairments resulting in LPS introduction into the CV system.
AIM : The aim of the study was to investigate the effect of low physiological levels of systemic LPS exposure on the CV system, of male Sprague-Dawley rats over a ten-day period. Manuka honey was introduced as a possible mopping agent for the effects of LPS on the CV system.
STUDY DESIGN : Twenty-four 10-week-old male Sprague-Dawley rats (average weight: 250-300 g) were randomly divided into four groups. The groups included rats exposed to Phosphate buffer-saline, phosphate buffered-saline and Manuka honey, LPS only as well as LPS and Manuka honey. The animals were housed for 19 days, in which the animals were given daily subcutaneous injections. The Manuka honey administered to the control and experimental groups received the Manuka honey solution through oral gavage starting on the 11th day for a seven-day period.
METHODS : In this study we examined the CV tissue of the animals through light microscopy and transmission electron microscopy. The total cholesterol levels were also measured by using the QuickDetectTM total cholesterol (Rat) ELISA assay.
Results: Myocardial LPS exposure resulted in cardiac myofibril damage and mitochondrial cristae destruction. The results indicated that Manuka honey may have alleviated some of this damage. However, the treatment failed to prevent mitochondrial cristae destruction. Lipopolysaccharide exposure to aortic tissue resulted in cellular abnormalities, elastic fragmentation and collagen deposition. Manuka honey administration resulted in the reduction of cellular abnormalities and elastin fragmentation in the aorta however, the treatment induced collagen depletion.
CONCLUSION : The aorta and cardiac muscle are vulnerable to the effects of low levels of systemic LPS exposure. Exposure resulted in elevation in cardiac and aortic cellular and elastin destruction that may possibly conclude in CV disease long term. In addition, Manuka honey serves as an insufficient remedy to counteract the harmful effects of LPS on the CV system.
