Doxorubicin (DOX) is a potent chemotherapeutic agent. Unfortunately, due to the incidence of dose-dependent cardiotoxicity, its clinical usage is hampered. Natural products are gaining popularity as a means of preventing DOX-induced cardiotoxicity. In the present study, we investigated the cardiotoxic effects of DOX and assessed the potential ameliorative effects of Achillea fragrantissima extract, its combined ethyl acetate/ n. butanol (EtOAc-Bu) fraction, and vitamin E in adult male albino rats. Rats were randomly divided into five groups: Control, DOX, DOX + A. fragrantissima crude extract, DOX + its (EtOAc-Bu) fraction, DOX + Vitamin E. A single dose of DOX (15 mg/kg) was given intraperitoneally (ip) in each group except the control. Rats were assessed before scarification for arterial blood pressure and ECG recordings. Serum and heart tissue were collected for biochemical, and histopathological assessment. Pre-treatment with vitamin E, A. fragrantissima crude extract, and its (EtOAc-Bu) fraction ameliorated DOX-induced cardiotoxicity, in varying degrees and with varying significance, as evidenced by reversing the DOX-induced ECG changes, reducing serum cardiac enzymes, and improving DOX-induced histopathological changes. All the suggested protective measures, in varying degrees and with varying significance, reduced the oxidative stress, lipid peroxidation, and apoptosis markers (reduced NO, and MDA, down-regulated mRNA expression of both iNOS and caspase-3), and elevated the antioxidants markers (GR, SOD, and TAC). We concluded that such suggested natural products might offer a promising chemo-preventive approach against cardiotoxicity induced by DOX.

Injection of adipose-derived stem cells (ADSCs) into the injured tunica albuginea (TA) may prevent fibrosis, restore the balance between pro- and antifibrotic pathways, and potentially mitigate erectile dysfunction caused by abnormal TA healing. To assess the potential role of ADSC injection on structural, ultrastructural, functional, and molecular changes in surgically induced trauma of the rat’s TA. Forty adult male albino Wistar rats were divided into 5 groups of 8 rats each: group 1, sham; group 2, injury to TA without treatment; group 3, injury to TA and suture repair; group 4, injury to TA and injection of ADSCs without suture repair; group 5, injury to TA followed by injection of ADSCs and suture repair. After 6 weeks, all groups were subjected to functional, histologic, and ultrastructural examination and molecular expression of healing growth factors. The intracavernous pressure (ICP; mean ± SD) was 114 ± 2, 32 ± 2, 65 ± 2, 68 ± 2, and 111 ± 2 mm Hg in groups 1 to 5, respectively. There were significant differences in ICP between each of groups 3 to 5 and group 2 (P < .05), and groups 3 and 4 each had significant differences with group 1 (P < .05). No significant difference in ICP occurred between groups 3 and 4 (P > .05). There were significant histologic and ultrastructural alterations in tunical tissues from group 2; however, these changes were markedly less in group 5 in terms of lower levels of fibrotic changes, elastosis, and superior overall neuroendothelial expression. Groups 3 and 4 showed improved structural and ultrastructural parameters when compared with group 2. Group 5 demonstrated lower levels of transforming growth factor β1 and basic fibroblast growth factor expression. This experimental model may encourage administration of ADSCs to prevent the deleterious effects of trauma to the TA. Injecting ADSCs can improve the healing process and erectile dysfunction in a rat model following TA injury, and combining ADSC injection with surgical suturing resulted in superior outcomes. The main limitation was the absence of long-term ICP measurements and a longer follow-up period that may provide further insight into the chronic phase of the healing process. ADSC injection may prevent structural, ultrastructural, functional, and molecular alterations in surgically induced trauma of the rat’s TA and enhance the effect of tunical suturing after trauma.

Cardiac Autonomic Neuropathy (CAN) is a major chronic complications of DMII. Clinical investigations have revealed that uncontrolled DM II is frequently associated with lower levels of BDNF. This study assessed whether diminished BDNF level is the reason of CAN caused by DM II and if swimming aerobic exercise can increase BDNF level to ameliorate that CAN . Sixty rats were divided into six groups. Group I; Normal (N), Group 2; BDNF blocker, Group 3; DM II, Group 4; DM II + BDNF, Group 5; DM II + Swimming exercise and Group 6; DM II + Swimming exercise + BDNF blocker. Induction of DM II was done by intraperitoneal injection of 180 mg/kg of Nicotinamide 30 minutes before injection of 50 mg/kg Streptstozin. Swimming exercise began with a 1-week adaptation with gradual increase of swimming duration until reaching 1h swimming/day at the end of the 1st week. Then, a 7-weeks training program with 5 days/week swimming was followed. The duration of the experiment was 8 weeks during which the following parameters were measured: body weight, random blood glucose “RBG” level, plasma insulin level, heart rate “HR”, systolic blood pressure “SBP”, heart rate variability “HRV”, baroreflex sensitivity “BRS”, vascular sympathetic tone “VST” and plasma BDNF. Results revealed that BDNF significantly improved RBG level, HRV, VMT and BRS. Swimming exercise significantly increases plasma BDNF level and also improved CAN. Conclusively, BDNF can be used as a treatment regimen for CAN. Also swimming exercise has great therapeutic effect on CAN maybe by producing BDNF.