Natural Reno-Protective Agents against Cyclosporine A-Induced Nephrotoxicity: An Overview.
Sabrin Ragab Mohamed IbrahimHossam Mohamed AbdallahAli M El HalawanyGamal Abdallah MohamedAisha A AlhaddadWaad A SammanAli A AlqarniAkaber T RizqKholoud F GhazawiRiham Salah El-DinePublished in: Molecules (Basel, Switzerland) (2022)
CA (cyclosporine A) is a powerful immunosuppressing agent that is commonly utilized for treating various autoimmune illnesses and in transplantation surgery. However, its usage has been significantly restricted because of its unwanted effects, including nephrotoxicity. The pathophysiology of CA-induced kidney injury involves inflammation, apoptosis, tubular injury, oxidative stress, and vascular injury. Despite the fact that exact mechanism accountable for CA's effects is inadequately understood, ROS (reactive oxygen species) involvement has been widely proposed. At present, there are no efficient methods or drugs for treating CA-caused kidney damage. It is noteworthy that diverse natural products have been investigated both in vivo and in-vitro for their possible preventive potential in CA-produced nephrotoxicity. Various extracts and natural metabolites have been found to possess a remarkable potential for restoring CA-produced renal damage and oxidative stress alterations via their anti-apoptosis, anti-inflammatory, and antioxidative potentials. The present article reviews the reported studies that assess the protective capacity of natural products, as well as dietary regimens, in relation to CA-induced nephrotoxicity. Thus, the present study presents novel ideas for designing and developing more efficient prophylactic or remedial strategies versus CA passive influences.
Keyphrases
- oxidative stress
- diabetic rats
- drug induced
- high glucose
- protein kinase
- reactive oxygen species
- dna damage
- cell death
- anti inflammatory
- induced apoptosis
- endoplasmic reticulum stress
- stem cells
- ischemia reperfusion injury
- endothelial cells
- systematic review
- ms ms
- coronary artery disease
- cell proliferation
- cell cycle arrest
- mesenchymal stem cells
- mass spectrometry
- molecular dynamics
- atrial fibrillation
- climate change