ABSTRACT
Background: Diabetic erectile dysfunction (DED) is a significant consequence of diabetes mellitus, and it is a multifactorial phenomenon that has no definitive treatment until now. Many therapeutic options provide symptomatic improvement rather than addressing the underlying etiology or restoring normal function. Stem cell (SC) therapy represents a potential hope in DED management. It is well established that the regenerative effect of stem cells can be attained by their paracrine action and their ability to differentiate into many cell lineages, including endothelial and smooth muscle cells. Hence, we tried to compare the effects of transplantation of urine-derived stem cells (USCs) or their lysate (USC-L) into the corpora cavernosa (CCs) of rats with DED. Materials and Methods: A total of 55 adult male Wistar rats were included in this study. USCs were obtained from ten healthy rats. Another ten rats did not subject to any intervention and served as a control (group I). Type 2 DM and DED were induced in the remaining 35 rats, but DED was tested and proved in only 24 rats, which were randomly divided into three groups (n = 8 in each). The DED group (group II) and either USCs (2 × 106 cells) or their lysate (200 µl) were transplanted into the CCs of each rat in the other two groups (groups III and IV), respectively. Results: Although the DED rats exhibited deterioration in all copulatory functions as compared to the control group, our histopathological, immunohistochemical, and morphometric results revealed that both USCs and USC-L have significantly restored the cavernous spaces, the ultrastructures of the endothelium that line the cavernous spaces, collagen/smooth muscle ratio, and the mean area percentage of α-SMA in the CCs as compared to DED rats. A respectable number of USCs was detected in the CCs of group III at the 4th week after transplantation, but this number significantly declined by the 8th week. Conclusion: Both USCs and USC-L can repair the structure and ultrastructure of CCs and improve the copulatory functions in the DED rat model. However, USC-L could be better used in DED to guard against the strange behavior of USCs after transplantation and their decreased survivability with time.
ABSTRACT
Oncotherapeutics like doxorubicin can affect male gonads; as a result, it leads to infertility. This work was conducted to demonstrate the toxic effects of doxorubicin on testes of male albino rats. Fifty male albino rats aged 5-7 weeks were used in this study. The animals were randomly separated into 5 sets (each set containing ten rats). Group I received saline (i.p.) for 4 weeks. Group II was given doxorubicin (DOX), 5 mg/kg BW (i.p.) once/week for 4 weeks. Groups III and IV were treated in the same way as the DOX group, left for one week without medication, and then injected with mesenchymal stromal cells (MSCs) or human placental extract (HPE) therapy in a single dose of 5 × 106 in 200 ml PRP/week or 40 µl placental extract for 4 weeks via the caudal vein. Group V rats were treated in the same way as the DOX group also, left for one week without medication, and then injected with MSC+HPE. A significant decrease in serum testosterone, FSH, and LH levels was observed in rats treated with DOX compared to the control group. A significant elevation was recorded in rats treated with DOX+MSC or DOX+HPE when compared with the DOX group only. Rats that were given MSC+HPE after DOX intoxication showed a significant increase in hormone levels when compared to rats treated with either MSC or HPE. Light and electron microscopic examinations revealed that DOX intoxication initiated degenerative and necrotic changes in seminiferous tubules associated with partial or complete cessation of spermatogenesis. These effects were reversed by the effect of MSC or HPE. Coadministration of MSC and HPE even showed further improvement. Finally, we can say that doxorubicin has a deleterious impact on rat testes; however, therapeutic effects can be induced through MSC and/or HPE administration.
Subject(s)
Doxorubicin/toxicity , Mesenchymal Stem Cell Transplantation/methods , Placental Extracts/administration & dosage , Testis/physiology , Animals , Combined Modality Therapy , Female , Follicle Stimulating Hormone/blood , Humans , Luteinizing Hormone/blood , Male , Mice , Placental Extracts/pharmacology , Pregnancy , Rats , Testis/drug effects , Testosterone/bloodABSTRACT
Cisplatin is broadly used in the treatment of malignancies. However, the high incidence of nephrotoxicity following cisplatin use deters its clinical utility. Former studies have shown that the essential oils, obtained from Citrus limonia demonstrated significant anti-inflammatory and antioxidant effects. The aim of the current work was to evaluate the protective effects of Citrus limonia oil against cisplatin-induced nephrotoxicity. Thirty-two adult male mice were divided into four groups, eight mice each. The control group received distilled water, and the second group received a single intraperitoneal injection of cisplatin (20 mg/kg), while the third and fourth groups received cisplatin plus Citrus limonia oil at 100 or 200 mg/kg for 10 days, respectively. GC-MS analysis showed that the major components in Citrus limonia oil were D-limonene, 5-methyl-pentadecane, (n)-menthol, 3,7-dimethyl-(E)-2,6-octadienal, 3,7-dimethyl-2,6-octadienal, and nonadecane. Biochemical analysis showed that cisplatin intoxication was associated with significantly increased (p < 0.05) serum levels of urea and creatine and pro-inflammatory cytokines, as well as augmented renal tissue oxidative stress. Light microscopic examination showed loss of renal architecture, atrophied glomeruli, interstitial hemorrhage, dilated cortical tubules with cast formation, and excessive collagen production. Electron microscopic examination revealed compressed and karyorrhectic endothelial nuclei with chromatin condensation in the glomeruli, accumulation of mesangial matrix, and obliteration of glomerular blood capillaries. Co-administration of Citrus limonia oil attenuated these effects in renal histopathological, morphometric, and ultrastructural examinations, frequently in a dose-dependent manner. In conclusion, Citrus limonia oil can ameliorate the toxic effect of cisplatin on mice kidneys, probably through its antioxidant and anti-inflammatory effects.
Subject(s)
Cisplatin , Citrus , Animals , Antioxidants/metabolism , Cisplatin/toxicity , Creatinine/metabolism , Kidney/metabolism , Male , Mice , Oxidative StressABSTRACT
Diazinon has been reported to produce oxidative stress and adverse effects on many organs. In contrast, propolis components behave as hydrophilic antioxidants. To evaluate the protective effect of propolis on diazinon-induced nephrotoxicity in adult male albino rats, eighty adult male albino rats were divided randomly into four groups: control, diazinon treated, propolis treated and diazinon plus propolis groups. Control group were divided into two subgroups: the first was not given any treatment and the second one received 1.5 ml of sterile distilled water through intra-gastric tube daily for 4 consecutive weeks. The diazinon group was treated with 10 mg/kg through intra-gastric tube, daily for 4 weeks. The propolis group received 50 mg/kg through intra-gastric tube, daily for 4 weeks. The diazinon-plus-propolis group was treated with the same doses as previous groups. Kidneys were removed and processed for haematoxylin and eosin, caspase-3 immunostaining and electron microscopic examination. Renal tissues of diazinon-treated rats showed histopathological and ultrastructural changes such as shrunken glomerulus, hemorrhage, congestion, increased Bowmans space, inflammatory infiltration, degenerated tubules with vacuolated epithelial cell lining, pyknosis and necrotic debris. Rats of the diazinon-plus-propolis group showed a marked reduction in these pathological features. We conclude that propolis can ameliorate the nephrotoxicity induced by diazinon
No disponible
Subject(s)
Animals , Rats , Propolis/pharmacokinetics , Diazinon/adverse effects , Renal Insufficiency/prevention & control , Disease Models, Animal , Protective Agents/pharmacokinetics , Kidney GlomerulusABSTRACT
Oxidative stress induced by free radicals is known to be a common cause of liver damage and hepatic fibrosis. Anise oil and its compounds have been identified to have antioxidant, anti-inflammatory and antifibrinogenic properties that may play a role in the management of hepatic disorders and promote liver regeneration. Thus, the purpose of the study was to evaluate the effects of anise oil on hepatotoxicity induced by carbon tetrachloride in adult male albino rats. Sixty male albino rats were divided into control group, CCL4-treated group that was injected with 1 mg /kg CCL4 intraperitoneally (ip), CCL4+anise oil-treated group that was injected with 1 mg /kg of CCL4 and 0.5 ml/ kg of anise oil (ip), and anise oil-treated group that was injected with 0.5 ml/kg of anise oil. Animals received treatment for 4 weeks and sacrificed 24 hours after the last administration. Livers were removed and processed for light and electron microscopy analysis. The CCL4-treated group revealed loss of normal architecture of hepatic lobules, steatosis, necrosis, cholestasis, portal congestion and progressed grading of lobular inflammation, ballooning degeneration and fibrosis. On the other hand, the CCL4 + anise group showed reduced liver damage and increased signs of regeneration. We conclude that anise oil has a protective effect on liver damage caused by CCL4and promotes liver regeneration (AU)
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