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ABSTRACT

  • 1Moshape MTP,
  • 2van Hoogland-van Heerden M ,
  • 3Mokoena TS ,
  • 4Millen AME ,
  • 5Mokotedi L
  • 1Cardiometabolic Health Research Unit, Department of Physiology, Sefako Makgatho Health Sciences University, Pretoria
  • 2Cardiometabolic Health Research Unit, Department of Physiology, Sefako Makgatho Health Sciences University, Pretoria
  • 3Integrated Molecular Physiology Research Initiative (IMPRI), School of Physiology, University of Witwatersrand, Johannesburg
  • 4Integrated Molecular Physiology Research Initiative (IMPRI), School of Physiology, University of Witwatersrand, Johannesburg
  • 5Cardiometabolic Health Research Unit, Department of Physiology, Sefako Makgatho Health Sciences University, Pretoria

Background

Systemic inflammation in rheumatoid arthritis (RA) contributes to cardiometabolic impairments. While glucocorticoids (GCs) effectively manage inflammation, their impact on inflammation-induced cardiometabolic dysfunction remains unclear. This study investigated the effects of GCs on cardiometabolic function in a collagen-induced arthritis (CIA) rat model.

Method

Male Sprague Dawley rats were assigned to control, CIA, GC, and CIA+GC groups (n=9 per group). Arthritis was induced in the CIA and CIA+GC groups using bovine type-II collagen emulsified in incomplete Freund’s adjuvant. Following signs of inflammation, the CIA+GC and GC groups received prednisolone daily for six weeks. Body mass, arthritis scores, cardiac function, left ventricular (LV) collagen accumulation, circulating concentrations of high sensitivity-C-reactive protein (hs-CRP), and cholesterol were assessed.

Result

CIA+GC rats had lower arthritis scores and hs-CRP levels than CIA rats and higher cholesterol levels than control and GC rats (p<0.01). CIA+GC rats had higher LV collagen area fraction and relative wall thickness than control rats (p<0.05) with impaired diastolic function indicated by reduced lateral e’ and e’/a’ ratio and increased filling pressures (E/e’) (p<0.01). Global longitudinal strain and strain rate were reduced in CIA+GC rats than in control rats (p<0.05). High cholesterol levels were associated with increased relative wall thickness, E/e’ ratio, and GLS and reduced lateral e’, independent of hs-CRP (p<0.05).

Conclusion

While GC treatment reduced inflammation in CIA rats, it did not prevent hypercholesterolaemia, concentric remodelling, cardiac fibrosis, diastolic, and preclinical systolic dysfunction. Elevated cholesterol was independently linked to cardiac alterations, suggesting it drives these adverse changes.
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PRESENTING AUTHOR

Ms. Madikadike Moshape, MSc Medicine (Physiology), BSc Honours in Medical sciences (Physiology), BSc in Human Physiology, Genetics and Psychology.

Postgraduate Student, Sefako Makgatho health Sciences University

Madikadike Tumiso Pinky Moshape is a highly dedicated and accomplished academic professional.

She holds an MSc Medicine in Physiology (Cum Laude) and a BSc Honours in Medical Sciences (Physiology) (Cum Laude) from Sefako Makgatho Health Sciences University, as well as a BSc in Human Physiology, Genetics, and Psychology from the University of Pretoria. Her commitment to academic excellence has earned her several prestigious accolades, including membership in the Golden Key International Honour Society and the Stars Mentorship Program Award.

She has presented her research at esteemed scientific gatherings, including the Physiology Society of Southern Africa (PSSA, 2024) and the Biomedical Research & Innovation Platform Conference (BRIP, 2023 and 2024). These accolades and engagements underscore her commitment to academic excellence, scientific contribution, mentorship, and professional growth.

/ends
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