Nephroprotective Effect of Telmisartan in Rats with Ischemia/Reperfusion Renal Injury

Abstract

We investigated the protective effect of telmisartan, an angiotensin II receptor antagonist, against ischemia/reperfusion renal injury in rats. Bilateral ischemia was induced by clamping both renal vascular pedicles for 45 min followed by reperfusion for 3 h. Untreated rats exposed to ischemia/reperfusion showed significant elevations in blood urea nitrogen and serum creatinine levels, renal tissue levels of malondialdehyde, tumor necrosis factor-α and nitric oxide, and caspase-3 activity. This was associated with significant decreases in renal reduced glutathione level, catalase and superoxide dismutase activities. Also, significant increases in serum and renal tissue levels of homocysteine were detected following ischemia/reperfusion. Pre-ischemic treatment with telmisartan (0.3 mg/kg/day, i.p.) for 7 consecutive days significantly attenuated the increases in blood urea nitrogen, serum creatinine, renal malondialdehyde, tumor necrosis factor-α, nitric oxide, caspase-3 activity, and serum and renal homocysteine levels, and significantly restored the renal antioxidant defenses. In addition, light and electron microscopic examinations revealed that telmisartan pre-treatment markedly ameliorated ischemia/reperfusion-induced renal tissue damage. It was concluded that telmisartan, through its antioxidant, anti-inflammatory and antiapoptotic effects, can be considered a potential candidate to protect against acute ischemia/reperfusion renal injury.

Investigation of the effect of telmisartan on experimentally induced peripheral nerve injury in rats

“…The decrease in caspase-3 expression in response to the administration telmisartan demonstrates that it prevented nerve cells from injury by decreasing the apoptotic pathway. In line with our study, previous data reported that telmisartan significantly attenuated increases in caspase-3 activity in renal injury, suggesting that telmisartan, through its anti-inflammatory and antiapoptotic effects, can be considered a potential candidate to protect against traumatic injuries [37]. In addi-tion, neuroprotective effects of pioglitazone, a PPAR-γ ligand of telmisartan, were shown to be mediated by inhibition of postischemic inflammation, neuronal degeneration, and apoptosis; by protection of neurons against ischemic injury; and by promotion of neuronal regeneration [38].…”

Telmisartan Attenuates Diabetic Nephropathy by Suppressing Oxidative Stress in <b><i>db/db</i></b> Mice

“…Other investigators have reported that telmisartan also suppressed oxidative stress in doxorubicin-induced nephrotoxicity [18], ischemia/reperfusion injury [19], and streptozotocin-induced diabetic nephropathy [20]. However, little is known about the therapeutic potential of telmisartan in type 2 diabetic nephropathy associated with obesity.…”

“…Although the mechanisms are not fully understood, one attractive possible mechanism is that telmisartan may have antioxidative stress effects. We and other investigators have reported that the renoprotective effects of telmisartan are at least partly mediated by reducing oxidative stress in a variety of animal models including unilateral ureteral obstruction [17], doxorubicin-induced nephrotoxicity [18], ischemia/reperfusion injury [19], and type 1 diabetic nephropathy [20]. To address whether telmisartan suppresses oxidative stress and prevents diabetic nephropathy, we administered telmisartan to db/db mice, a mouse model of type 2 diabetes and obesity.…”

Lysophosphatidic Acid and Lovastatin Might Protect Kidney in Renal I/R Injury by Downregulating MCP-1 in Rat

“…Molecules and peptide were reported to have protective effect on renal function in I/R injury. [13][14][15] Mesenchymal stem cells and human hematopoietic stem/progenitor cells were used to treat rat renal I/R injury, which facilitates repairing of renal tissue. [16][17][18] It has been demonstrated that lysophosphatidic acid (LPA) may protect renal function by antiinflammatory, inhibiting expression of tumor necrosis factor, inflow of neutrophilic granulocyte, and activation of complement.…”