ABSTRACT
BACKGROUND: Cyclophosphamide (CP), as a chemotherapy drug, causes severe damage in testicular tissue through producing free radicals. Cerium oxide nanoparticles (NC) exhibit antioxidant and anti-inflammatory properties. The purpose of this study was to investigate the protective effect of NC on CP-induced testicular damage in mice. METHODS: In this experimental study, thirty-two male mice were divided into four groups (eight mice in each group). The control group was received intraperitoneally (IP) normal saline, NC group was received NC for three consecutive days (100 µg/kg, IP), CP group was received CP (200 mg/kg, IP), and the CP + NC group received NC, three consecutive days before receiving CP. After 2 days, testicles were assessed for biochemical, histomorphometrical, histopathological, and immunohistochemical analyses. RESULTS: CP administration caused statistically significant increases in sperm abnormality, malondialdehyde, protein carbonyl levels, reactive oxygen species, level and apoptosis, and decreases in sperm count, sperm viability, testosterone, glutathione activity, the mean thickness of the germinal epithelium, diameter of seminiferous tubules in mice. Degeneration, necrosis, arrest of spermatogenesis, congestion, and atrophy in testicular tissue confirmed the low Johnsen's Testicular score in CP group. Administration of NC significantly ameliorated the CP-induced adverse effects on testis compared with the CP group. In addition, pretreatment mice with NC significantly reduced caspase-3 immunoreactivity induced by CP in testis. CONCLUSIONS: This study showed that NC with scavenging free radicals and antiapoptotic properties enable to reduce the side effects of CP in the testicular tissue.
ABSTRACT
BACKGROUND: The human amniotic membrane (HAM) is a suitable and effective scaffold for cell culture and delivery, and adipose-derived stem cells (ADSCs) are an important source of stem cells for transplantation and chondrogenic differentiation. OBJECTIVE: To assess the practicability of a cryopreserved HAM as a scaffold in cell proliferation and differentiation in vitro. MATERIALS AND METHODS: In this experimental study, adipose tissue samples were harvested from the inguinal region of male patients aged 15-30 years. Flow cytometry was used to identify CD31, CD45, CD90, and CD105 markers in adipose stem cells. HAM was harvested from donor placenta after cesarean section, washed, trypsin-based decellularized trypsinized decellularized, and used as a scaffold via three methods: 1) ADSCs were differentiated into chondrocytes on cell culture flasks (monolayer method), and after 14 days of culture, the cells were transferred and cultured on both sides of the HAM; 2) ADSCs were cultured and differentiated directly on both sides of the HAM for 14 days (scaffold-mediated differentiation); and 3) chondrocytes were differentiated with micromass culture for 14 days, transferred on HAM, and tissue slides were histologically analyzed qualitatively. RESULTS: Flow cytometry confirmed the presence of mesenchymal stem cells. Histological findings revealed that the cells adhered and grew well on the stromal layer of HAM. Among the three methods, scaffold-mediated differentiation of ADSCs showed the best results. CONCLUSION: ADSCs have excellent attachment, viability, and differentiation capacity in the stromal side of HAM. Additionally, the direct culture and differentiation of ADSCs on HAM is more suitable than the culture of differentiated cells on HAM.
ABSTRACT
BACKGROUND: Sodium arsenate (As), a toxic substance with induced oxidative stress, lead to hepatotoxicity. Olive oil (OO) with antioxidant property has protective effect on toxicity. The aim of this study was to investigate protective effect of OO on sodium As-induced hepatotoxicity in mice. SUBJECTS AND METHODS: In this experimental study, 32 adult male BALB/c mice were divided randomly into four groups: control group (received only normal saline, the same volume as other groups), OO (0.4 mL/day, gavage), sodium As (15 mg/kg, gavage), and OO + sodium As (received OO 1 h before sodium As). Drugs were given for 30 consecutive days. After the last receipt of the drugs, oxidative stress parameters [malondialdehyde (MDA), glutathione (GSH)] in tissue, liver function parameters [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP)] in serum, ferric reducing ability of plasma (FRAP) in plasma, and histopathological assays were performed. RESULTS: Sodium As induced hepatic injury as indicated by significant increase in AST, ALT, ALP, and LDH in serum and pathologic evidences. It also induces hepatic oxidative stress biomarkers as indicated by significant increase in levels of MDA and significant decrease in FRAP and GSH concentration. OO administration significantly improved oxidative stress parameters, histopathological changes, and enzymatic markers of liver injury. CONCLUSIONS: It was concluded that antioxidant activity of OO has hepatoprotective effect on As-induced hepatic injury.
