Protective effect of Curcuma longa extract on acetaminophen induced nephrotoxicity in mice

Acetaminophen is a commonly used analgesic and antipyretic agent which, in high doses, causes liver and kidney necrosis in man and animals. Curcuma longa has been reported to have anti oxidant and hepato-protective properties. In this study the protective effect of Curcuma longa extract on acetaminophen induced nephrotoxicity has been evaluated. Sixty NMRI male mause were randomly divided into 6 groups. Control group received normal saline. Curcuma longa group received 1000 mg/kg of the extract of the plants, positive control group received 500 mg/kg acetaminophen. Acetaminophen and Curcuma longa extract at doses of 400, 800 and 1000 mg/kg were administered to the tested groups [T[1] T[3]] at the same time. The jugular arteries of the mice were cut for biochemical testes after 48 hours and the kidney removed in 10% formalin solution for histopathology testes. BUN, Cr and Uric acid reduced significantly in the T[3] group [p < 0.05]. Necrosis of kidney reduced in test groups especially in T[3] group. The results of this study indicate that Curcuma longa extract may protect kidney against acetaminophen - induced tubular necrosis in mice

[ 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

[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