Cisplatin (CIS) provides oxidative stress and inflammations in testicular tissues. Fenugreek seed extract (FSE) is a widely used herbal medicine with potent antioxidant and anti-inflammation properties. The purpose of this study was to investigate the protective effects and the possible mechanisms of FSE against CIS-induced testicular damage in rats. Adult male Wistar rats were given vehicle, single dose of CIS alone (10 mg kg(-1)), single dose of FSE alone or single dose of CIS followed by FSE (50, 100 or 200 mg kg(-1)) every day for 5 days. On day 6, oxidative stress and apoptotic testicular toxicity were evaluated. FSE attenuated both germ cell degenerations and apoptosis in seminiferous tubules in CIS-treated rats. Furthermore, FSE counteracted CIS-induced oxidative stress in rats as assessed by the restoration of superoxide dismutase and catalase activities and reduction in the myeloperoxidase activity and malondialdehyde levels in testes. CIS increased expressions of inducible nitric oxide synthase and nuclear factor-kappa B in testicular tissues. Importantly, treatment with FSE at all doses effectively alleviated all of these inflammatory parameters in testes. Based on these results, we concluded that FSE reduces CIS-induced reproductive toxicity in rats by the suppression of testicular oxidative stress, apoptosis and inflammations.

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Background: Memory disorders have been characterized by being a devastating long term incurable diseases with a huge social impact in addition to a diminished efficient available medical treatments. Deep Brain stimulation via using neuroprotective inducers for treatment of brain structure degenerative diseases such as Alzheimer's disease (AD) can be considered as being a promising successful therapy due to its various targets and underlying mechanisms for improving brain dysfunction. Objectives: The main aim of this study is to suggest therapeutic protocol having the potentials for restoring normal neurons diverse population and modifying neuropathological deposited hallmarks including both positive and negative lesions. Materials and Methods: Rats were divided into nine groups: (G1) control ;(G2) rats received LPS as a method of inducing nongenetically manipulated AD;(G3)AD rats received NaHS;(G4) AD rats received MSCs intracerebrally;(G5) AD rats received MSCs+NaHS;(G6)AD rats received kefir+GB;(G7)AD rats received MSCs+kefir+GB;(G8)AD rats received NaHS+kefir+GB; (G9) AD rats received MSCs+NaHS+kefir+GB. Results: AD induction resulted in down-regulation of CBS expression and GSH brain tissue level accompanied with overexpression in amyloid-β protein, MAPK, tau protein, ACAT expression and MDA brain tissue level in addition to elevated caspase-3 serum level. Conclusion: The implantation of amyloid reliving therapy that do have a wide clinical impact if initiated at benign plaques stage before irreversible brain damage occurs. The following effects have been observed following the administration of suggested medical protocol where a decrease in AD pathological deposited hallmarks has been observed with maintaining inflammatory brain factors by functioning as a potent neuroregenerative.

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