Publications by authors named "Teimour Ghazizadeh"
Due to the association of oxidative stress and telomere shortening, it was aimed in the present study to investigate the possibility whether cyclosporine-A exerts its nephrotoxic side effects via induction of oxidative stress-induced renal telomere shortening and senescent phenotype in renal tissues of rats. Renal oxidative stress markers, 8-hydroxydeoxyguanosine, malondialdehyde, and protein carbonyl groups were measured by standard methods. Telomere length and telomerase activity were also evaluated in kidney tissue samples.
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- Cyclosporine A (CsA) can cause nephrotoxicity, which is harmful to kidneys, and its effects are linked to oxidative stress; Valsartan (Val), an angiotensin receptor blocker, may help protect kidneys from these effects.
- In a study with rats, Val was found to counteract the kidney damage caused by CsA by maintaining levels of Klotho, a protein that supports kidney health, and reducing markers of oxidative stress.
- The results suggest that Valsartan could be a beneficial treatment alongside CsA in preventing kidney damage by possibly enhancing Klotho expression and reducing oxidative stress levels.
Introduction: Calcineurin inhibitor nephrotoxicity is major problem after organ transplantation. It is multifactorial, but oxidative stress may have an important role in this process. It has been shown that angiotensin II receptor blockers have renoprotective effects but their molecular mechanism is largely unknown.
View Article and Find Full Text PDFNephrotoxicity as a side effect caused by the immunosuppressive drug, cyclosporine-A (CsA), can be a major problem in transplant medicine. Oxidative stress may play an important role in the CsA-induced nephrotoxicity. It has been shown that the antihypertensive drug, valsartan (Val), has also renoprotective effects but, its molecular mechanism is largely unknown.
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