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Nanomaterials in Cardio Protection
Published in Parimelazhagan Thangaraj, Lucindo José Quintans Júnior, Nagamony Ponpandian, Nanophytomedicine, 2023
A healthy heart is imperative for a steady flow of blood to carry oxygen and essential compounds required by numerous cells, tissues and organs throughout the body. The performance of the heart can be disturbed by diet, smoking, alcohol, infection and genes. Disease conditions where blood flow is obstructed are termed as ischemia. Ischemic diseases can affect different organs and tissues in the body. Ischemic heart disease, ischemic hepatitis, ischemic stroke and renal ischemia are some examples that occur in the heart, liver, brain and kidney, respectively. Cardiac diseases could occur as a single moiety or in combination with hypertension, drug-induced cardiac complications, diabetes, doxorubicin (DOX)-induced cardiomyopathy, age and many other factors.
The nephroprotective potential of diosgenin against ischemia-reperfusion acute renal damage via suppression of oxidative stress and downregulating inflammatory mediators
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Prachi Mishra, Deepa Mandlik, S Arulmozhi, Kakasaheb Mahadik
Acute renal damage is defined as a rapid and unpredicted decline in kidney physiology, causing accretion of nitrogen waste products like urea, uric acid and creatinine with or without affecting the diuresis process [1]. ARD is linked with a higher risk of morbidity and mortality and is resulted in manifold organ failure [2]. Research studies indicate that the overall incidence rate of ARD in hospital admitted patients was about 20% and 67% in intensive care unit patients [3,4]. Ischemic kidney damage may be resulted due to renal transplantation [4], partial nephrectomy [5], renal artery revascularization [6], trauma [7] and hydronephrosis [8]. Various undesirable situations like elevated blood pressure and chronic kidney failure may result in renal ischemia. Further kidney tissue damage is prevented by the restoration of kidney blood circulation, reperfusion frequently aggravates kidney dysfunction encouraged by reperfusion injury, a situation called as oxygen paradox [9]. Renal ischemia is a multiphase disease, prompting deficiency in oxygen, nutrient source and removal of waste products from the kidney. Successive reperfusion encourages dysfunction of endothelial cells and will be the main reason for renal damage [10–12]. Subsequently, I/R injury resulted in inflammation and oxidative stress, causing apoptosis and necrosis of renal tubular cells: provoking deterioration of kidney role. Hence, primary prevention and treatment of patients at high risk of acute kidney injury are paramount important [13]. Succeeding renal ischemia/reperfusion injury, the process of inflammation initiates as a consequence of cell injury. The cell injury results in the generation of molecular products which causes activation of kidney dendritic and parenchymal cells, initiating the secretion of cytokines and chemokines [14–16]. As well as renal ischemia resulted in accumulation of leukocytes at the site of injury leading to up-regulation of intracellular adhesion molecules-1 (ICAM-1) in vascular endothelium and secretion of inflammatory cytokines such as interleukin (IL)-1, IL-6 and Tumor necrosis factor-α (TNF-α) [17]. Furthermore, renal I/R injury augments the expression of inducible nitric oxide synthase and nitric oxide (NO) that leads to the formation of peroxynitrite radicals by reacting with reactive oxygen species. Also, it inhibits nitric oxide synthase enzyme with the declining formation of NO in renal endothelium and results in vascular endothelium constriction [18–20].