ABSTRACT
Objective: Hepatic cancer is known as primary liver cancer and hepatocellular carcinoma (HCC). Newly silver nanoparticles gained importance due to its advantages and multiple potential such as molecular imaging agent, antimicrobial, wound healing, anti-inflammatory and anticancer activity. The current study deals to assess therapeutic property silver nanoparticles (AgNPs) against diethylnitrosamine (DENA), and carbon tetrachloride (CCL4) induced hepatic cancer. Methods: Thirty male albino rats (200-250g) were distributed into four groups and hepatic cancer was induced with a single intraperitoneal dose of 200 mg/kg body weight of DENA. Two weeks later, animals received subcutaneous injections of CCl4 once a week in a dose of 3 ml/kg body weight for 6weeks. Serum biomarkers, antioxidants enzymes, inflammatory markers were evaluated to find the anti-proliferative potential of silver nanoparticles. Histological evaluation and microscopic reports were also done to document the results of the current work. Results: AgNPs significantly recover the serum marker enzymes of hepatic parameter AST, ALT, ALP, and total bilirubin and also decreased the levels of NO, IL-6 and TNF-α. Histopathological features also exhibited recovery of a hepatic architecture in cancer-induced rats. Moreover, the immunohistochemical investigation demonstrated that the levels of PCNA, and Caspase-3, which are hepatocarcinogenic markers, were significantly improved by AgNPs. Conclusion: These results concluded that AgNPs showed promising curing effects on hepatocellular ailments.
ABSTRACT
The present work aimed to study the relation between total testosterone serum levels [TTSLs] and temporal lobe epilepsy [TLE] in men, as decreased TTSL may favour the occurrence of TLE, sexual disorders commonly associated with it and is amenable to therapeutic manipulations. TTSLs were measured in [20] men with TLE and [20] age matched healthy controls. Significantly higher TTSLs were found in patients than controls, in patients receiving antiepileptics than untreated ones and in polypharmacy patients than monotherapy ones. Eleven of the patients had sexual desire or arousal disorders, [9] of them were receiving antiepileptics, [8] of these [9] had increased TTSLs. Ten [10] other patients with decreased TTSLs were evaluated for the presence of TLE which could not be discovered in any of them. It seems that decreased TTSL does not cause TLE. Antiepileptics may be responsible for both the change in TTSLs and sexual disorders in men with TLE as they may elevate TTSLs yet lower levels of the physiologically active free testosterone