Effect of Saxagliptin on Oxidative and Apoptotic Biomarkers in Doxorubicin- Induced Cardiac Injury in Comparison with Telmisartan Treated Rats

One of the most potent and effective drugs in the field of chemotherapy is doxorubicin. It has shown remarkable efficacy against multiple cancer targets. Despite the effectiveness of this treatment, an important drawback is the cardiotoxicity caused by doxorubicin. This limitation has led oncologists to explore potential ways to prevent or reduce this toxic side effect. We will investigate in this study whether saxagliptin and telmisartan have any protective effects on heart tissue. We will study their effects on oxidative stress and apoptotic indicators in particular. There were a total of 28 rats, with 7 animals in each of the four groups: First group(control group): seven rats in good health were given distilled water for fourteen days in a row before being sacrificed on the fifteenth day.Group 2 (positive group): Seven rats were given a 20 mg/kg intraperitoneal dose of doxorubicin HCl as a single dose. The rats were sacrificed after twenty-four hours. In the third group, rats took 10 mg/kg of saxagliptin orally for 14 days in a row. They received a single dosage of 20 mg/kg of Doxorubicin IP on day 15, and after 24 hours, they were slaughtered .In Group 4, seven rats were given 10 mg/kg of Telmisartan orally for 14 days in a row. Doxorubicin was administered intraperitoneally once at a dosage of 20 mg/kg on the fifteenth day. The rats were sacrificed after a day. Glutathione (GSH), malondialdehyde (MDA), creatinine kinase (CK-mb), and caspase 3 levels were quantified in several groups in this investigation. The doxorubicin treated group had a significantly lower GSH level compared to the saxagliptin and telmisartan groups (p<0.05). Likewise, when contrasted with the doxorubicin-treated group, the saxagliptin and telmisartan groups exhibited a substantial decrease in MDA levels (p<0.05). The doxorubicin treated group had significantly higher CK-mb levels compared to the saxagliptin and telmisartan groups (p<0.05). Finally, when comparing the groups treated with doxorubicin to those treated with saxagliptin and telmisartan, there was a substantial drop in caspase 3 levels (p<0.05). It is clear from our in vivo enzymatic analysis that saxagliptin and telmisartan show promise as doxorubicin cardiotoxicity protectants. Further research into their effects on cardiac biomarkers and anti-inflammatory capabilities, as well as further prospective preventative measures, should be undertaken in a long-term study.