[Protective effect of Carthamus tinctorius L. extract on acetaminophen induced nephrotoxicity in mice]

Background and Objective: Acetaminophen is a commonly used analgesic and antipyretic agent which, in high doses, causes liver and kidney necrosis in man and animals. Carthamus tinctorius L. [Safflower] is a colorful and cheap plant that used often instead of saffron. In this study, protective effects of Carthamus tinctorius L. aqueous extract on acetaminophen induced nephrotoxicity in mice were investigated

Methods: In this experimental study, forty adult NMRI male mice were randomly divided into five groups. Group 1 [control group] received normal salin for 15 days. Group 2 received 300 mg/kg Carthamus tinctorius L. extract for 15 days. Group 3 received normal salin for 15 days and 500 mg/kg acetaminophen was given in 15[th] day. Groups 4 and 5 received daily 150 and 300 mg/kg Carthamus tinctorius L. extract for 15 days, respectively, and acetaminophen was also given in 15[th] day. In 16[th] day, blood samples were taken for BUN [Blood Urea Nitrogen], Cr [Creatinine] and Uric acid tests, and the mice kidneys were removed for histopathology assessments

Results: Acute renal necrosis and BUN, Cr and Uric acid levels were significantly increased in acetaminophen treated mice [P<0.05]. BUN, Cr and Uric acid levels were significantly reduced in the Carthamus tinctorius L. treated groups in comparison to acetaminophen group [P<0.05] and this reduction was greater in group 5. Carthamus tinctorius L. extract also reduced tubular necrosis-induced by acetaminophen

Conclusion: Carthamus tinctorius L. extract have protective effects on acute renal injury induced by acetaminophen

[Metformin effect on the mouse pancreatic langerhans islets volume]

Metformin is a widely used medicine for treatment of type 2 diabetes. In this study, the effect of various doses of metformin on the mouse islets of langerhans volume was investigated. Twenty four C57BL/6 adult male mice weighting 30 +/- 5 gr were randomly divided into 4 groups. Normal saline was given to the control group [group 4] and the experimental groups [groups 1-3] received 75, 150 and 300 mg/kg metformin daily by intraperitoneal injection for seven days. One day after the last injection the mice were sacrificed by cervical dislocation and their pancreases were fixed in 10% formalin for histological studies. The volume of the islets of langerhans was estimated by using Cavalieri method. Volume of the islets of langerhans in doses of 75 and 150 mg/kg Metformin showed a nonsignificant difference in comparison to control group [P>0.05]. 300 mg/kg metformin treated mice showed a significant increase in islets of langerhans volume compared to the control group [P<0.05]. Metformin increases in the islets of langerhans volume in a dose-dependent manner. Increasing effects of Metformin on the islets of langerhans volume may be due to proliferation or hypertrophy of beta cells

[Effect of dexamethasone on Fas ligand expression in mouse testicular germ cells]

Apoptosis [programmed cell death] is an important regulatory event in spermatogenesis. Abnormally accelerated apoptosis in germ cells, may lead to an imbalance between cell proliferation and death, resulting in impairment in spermatogenic. Some studies have shown that glucocorticoids affect testialar homeostasis by decreasing of testosterone level. In the present study, the influence of dexametasone [Dex], a widely used glucocorticoid agent, on expression of FasL [Fas-Ligand] protein [a proapoptotic protein] in mouse testicular germ cells is investigated. Twenty-four adult male [6-8 weeks] mice were randomly divided into 3 groups. The first and second test groups received 2 and 7 mg/kg Dex per day, respectively, for 7 days. The control group received only saline daily for 7 days. One day after the final injection, the mice were sacrificed and the test groups were placed in formalin solution for immunohistochemistry studies. Positive immunoreactivity was calculated by H-score method. The results revealed that expression of FasL in seminiferous epithelium is spermatogenic stage dependent, and the stage VII was the most susceptible to Dex. FasL expression was observed only at stages VII-VIII of spermatogenic cycle in 2 mg/kg Dex treated group [P < 0.05]. H-score was significantly increased in all stages of 7 mg/kg Dex treated group [P < 0.05]. The number of spermatocytes decreased significanhy in this group. It appears that glucocorticoid agents such as Dex, induces apoptosis by affecting proapoptotic proteins

[ study of Bax protein expression in dexamethasone induced apoptosis in spermatogenic cells in mice]

Some studies have shown that glucocorticoids affect testis homeostasis by decreasing testosterone level. In this study the influence of dexamehasone [Dex], a widely used glucocorticoid drug, was evaluated on expression of Bax protein in mice testicular germ cells and spermatogenesis process. In this experimental study thirty five adult male mice randomly divided into 5 groups. Test groups [T1-T4] received 2, 4, 7 and 10 mg/kg Dex per day for 7 days, respectively. Control group received only saline daily for 7 days. Then the mice were sacrificed and their testes were incubated in formalin for immunohistochemistry and histology studies. T1 and T2 groups, which received 7 and 10 mg/kg Dex, showed significant decrease in the number of germ cells and somatic cells of testes, and also in the maturity of spermatogenesis [p<0.05]. Immunohistochemical studies showed that Dex with doses of 7 and 10 mg/kg significantly increased Bax expression at all stages of spermatogenesis cycle except stage IX. It seems that glucocorticoid drugs such as Dex induce apoptosis in testicular germ cells by affecting proapoptotic proteins and causing defect in spermatogenesis process