Abstract: The present study investigated the protective effect of
thymoquinone (TQ), against cadmium-induced kidney injury in rats.
Cadmium chloride (1.2 mg Cd/kg/day, s.c.), was given for nine
weeks. TQ treatment (40 mg/kg/day, p.o.) started on the same day of
cadmium administration and continued for nine weeks. TQ
significantly decreased serum creatinine, renal malondialdehyde and
nitric oxide, and significantly increased renal reduced glutathione in
rats received cadmium. Histopathological examination showed that
TQ markedly minimized renal tissue damage induced by cadmium.
Immunohistochemical analysis revealed that TQ markedly decreased
the cadmium-induced expression of inducible nitric oxide synthase,
tumor necrosis factor-α, cyclooxygenase-2, and caspase-3 in renal
tissue. It was concluded that TQ significantly protected against
cadmium nephrotoxicity in rats, through its antioxidant, antiinflammatory,
and antiapoptotic actions.
Abstract: The protective effect of hesperidin was investigated in
rats exposed to liver injury induced by a single intraperitoneal
injection of cyclophosphamide (CYP) at a dose of 150 mg kg-1.
Hesperidin treatment (100 mg kg-1/day, orally) was applied for seven
days, starting five days before CYP administration. Hesperidin
significantly decreased the CYP-induced elevations of serum alanine
aminotransferase, and hepatic malondialdehyde and myeloperoxidase
activity, significantly prevented the depletion of hepatic glutathione
peroxidase activity resulted from CYP administration. Also,
hesperidin ameliorated the CYP-induced liver tissue injury observed
by histopathological examination. In addition, hesperidin decreased
the CYP-induced expression of inducible nitric oxide synthase, tumor
necrosis factor-α, cyclooxygenase-2, Fas ligand, and caspase-9 in
liver tissue. It was concluded that hesperidin may represent a
potential candidate to protect against CYP-induced hepatotoxicity.
Abstract: The protective effect of thymoquinone (TQ) was investigated in rats exposed to testicular injury induced by sodium arsenite (10mg/kg/day, orally, for two days). TQ treatment (10mg/kg/day, intraperitoneal injection) was applied for five days, starting three day before arsenic administration. TQ significantly attenuated the arsenic-induced decreases of serum testosterone, and testicular reduced glutathione level, and significantly decreased the elevations of testicular malondialdehyde and nitric oxide levels resulted from arsenic administration. Also, TQ ameliorated the arsenic-induced testicular tissue injury observed by histopathological examination. In addition, TQ decreased the arsenic-induced expression of inducible nitric oxide synthase and caspase-3 in testicular tissue. It was concluded that TQ may represent a potential candidate to protect against arsenic-induced testicular injury.
Abstract: The possible therapeutic effect of cannabidiol, the major non-psychotropic Cannabis constituent, was investigated against acute hepatotoxicity induced by a single oral dose of acetaminophen (500mg/kg) in mice. Cannabidiol (two intraperitoneal injections, 5mg/kg, each) was given 1 hour and 12 hours following acetaminophen administration. Acetaminophen administration caused significant elevations of serum alanine aminotransferase, and hepatic malondialdehyde, and nitric oxide levels, and a significant decrease in hepatic reduced glutathione. Cannabidiol significantly attenuated the deterioration in the measured biochemical parameters resulted from acetaminophen administration. Also, histopathological examination showed that cannabidiol markedly attenuated ameliorated acetaminophen-induced liver tissue damage. These results emphasize that cannabidiol represents a potential therapeutic option to protect against acetaminophen hepartotoxicity which is a common clinical problem.