malealdehyde and Disease-Models--Animal

Exposure to hypobaric hypoxia causes oxidative stress, neuronal degeneration and apoptosis that leads to memory impairment. Though oxidative stress contributes to neuronal degeneration and apoptosis in hypobaric hypoxia, the ability for phenylethanoid glycosides of Pedicularis muscicola Maxim (PhGs) to reverse high altitude memory impairment has not been studied. Rats were supplemented with PhGs orally for a week. After the fourth day of drug administration, rats were exposed to a 7500 m altitude simulation in a specially designed animal decompression chamber for 3 days. Spatial memory was assessed by the 8-arm radial maze test before and after exposure to hypobaric hypoxia. Histological assessment of neuronal degeneration was performed by hematoxylin-eosin (HE) staining. Changes in oxidative stress markers and changes in the expression of the apoptotic marker, caspase-3, were assessed in the hippocampus. Our results demonstrated that after exposure to hypobaric hypoxia, PhGs ameliorated high altitude memory impairment, as shown by the decreased values obtained for reference memory error (RME), working memory error (WME), and total error (TE). Meanwhile, administration of PhGs decreased hippocampal reactive oxygen species levels and consequent lipid peroxidation by elevating reduced glutathione levels and enhancing the free radical scavenging enzyme system. There was also a decrease in the number of pyknotic neurons and a reduction in caspase-3 expression in the hippocampus. These findings suggest that PhGs may be used therapeutically to ameliorate high altitude memory impairment.

Topics: Aldehydes; Altitude Sickness; Animals; Antioxidants; Caspase 3; Disease Models, Animal; Dose-Response Relationship, Drug; Glutathione; Glycosides; Hippocampus; Hypoxia; Male; Maze Learning; Memory Disorders; Pedicularis; Rats; Rats, Wistar; Reactive Oxygen Species; Spatial Memory; Superoxide Dismutase

Raphanus sativus is reported to have a variety of biological activities. This work screened the hepato-protective and antioxidant activity of ethanol (ERS), and aqueous (ARS), extracts of leaves of Raphanus sativus in Carbon tetrachloride (CCl4), model in rats.. The extracts were subjected to antioxidant tests (Total reducing power and Total phenolic content), and preliminary phytochemical screening. A pilot study was done on 100 and 300 mg/kg extracts, form which 300 mg was chosen for further experiments. The albino rats (200-250 grams), were divided into 5 groups of 6 animals each (n=6). There were three control groups comprising of normal control (normal saline -1ml/kg), negative control group (CCl4 1ml/kg in olive oil in a ratio of 1:1 v/v), and positive control group (Silymarin 50mg/kg). The Test drugs were given in a dose of 300 mg/kg for both ERS and ARS extract for 7 days. Biochemical parameters (AST, ALT, Alkaline phosphatase, Total Bilirubin), histo-pathological examination of liver and in vivo antioxidant tests [CAT, GSH and MDA] were done.. The phytochemical study showed the presence of flavanoids, terpenoids, alkaloids, saponins and sterols. A dose dependent increase in the oxidative potential was observed in both the extracts with total phenolic content 70.1 and 44.4 GAE/g extract for ERS and ARS respectively. ERS 300mg/kg showed a significant (p<0.001) increase in levels of AST, ALT and alkaline phosphatase as compared to negative control (percentage hepatoprotection =45.3%) while ARS 300 mg/kg (p<.01) group showed 30% hepatoprotection. The GSH (p<0.001) and CAT (p<0.05) in ERS and ARS were significantly increased while MDA levels were decreased (P< 0.01), as compared negative control. The findings were confirmed histo-pathological examination.. The ethanol and aqueous extract of Raphanus sativus have partial hepatoprotection against CCl4 toxicity.

Topics: Alanine Transaminase; Aldehydes; Animals; Antioxidants; Aspartate Aminotransferases; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Female; Humans; Liver; Male; Phytotherapy; Plant Extracts; Plant Leaves; Protective Agents; Raphanus; Rats

The aim of the present study was to investigate the role of complement activation in the pathogenesis of neuropathic pain (NPP) induced by peripheral nerve injury. We modified a classical chronic constriction injury (CCI) model (mCCI), and verified its reliability in rats. Furthermore, reverse transcription-PCR and immunohistochemistry were conducted to investigate complement activation in the spinal dorsal horn and the effect of a complement inhibitor, cobra venom factor (CVF), on the behavior of the mCCI model rats. We found that rats in the mCCI group presented a better general condition, without signs of autophagy of the toes. Moreover, mCCI induced a significant increase (+40%) in the expression of component 3 (C3) mRNA in the spinal dorsal horn, which was associated with hyperalgesia. Correlation analysis showed a negative correlation between the mechanical pain threshold and the expression of C3 in the spinal cord. Administration of CVF reduced the occurrence of hyperalgesia in mCCI rats and nearly reversed the hyperalgesia. In addition, the mCCI rats exhibited significantly less spinal superoxide dismutase activity and significantly greater levels of maleic dialdehyde compared to the sham-operated rats. Transmission electron micrographs revealed mitochondrial swelling, cell membrane damage, and cristae fragmentation in the neurons of the spinal dorsal horn 14 days after mCCI. Mitochondrial swelling was attenuated in mCCI rats receiving CVF. The findings demonstrated that abnormal complement activation occurred in the dorsal horn of the spinal cord in rats with NPP, and C3 in the spinal dorsal horn could play an important role in the cascade reaction of complements that are involved in the development of hyperalgesia.

Topics: Aldehydes; Animals; Autophagy; Complement Activation; Complement C3; Disease Models, Animal; Disease Progression; Elapid Venoms; Gene Expression; Hyperalgesia; Male; Mitochondria; Neuralgia; Pain Threshold; Posterior Horn Cells; Rats; RNA, Messenger; Spinal Cord; Superoxide Dismutase

The model of lymphatostatic encephalopathy was established by occluding and removing profound cervical nodes in rats, and the kinetic alteration of nitric oxide (NO), maleic dialdehyde (MDA), free radical scavenger (CuZn-SOD) and arterial systolic blood pressure were determined on different days after the blockage. The results showed that the level of NO significantly decreased at 1 day (P<0.05) and further decreased at 3, 5 and 7 day (P<0.01). The levels of MDA at 1, 3, 5 and 7 day significantly increased, but the contents of CuZn-SOD significantly decreased compared with the control (P<0.01). There was negative correlation between the levels of MDA and CuZn-SOD, but there was no relationship between MDA an NO. Arterial systolic blood pressure decreased progressively after cervical lymphatic blockage. The results showed that NO, oxide free radicals and the disturbances of the cardiovascular regulation may play important roles in lymphatostatic encephalopathy.

Topics: Aldehydes; Animals; Blood Pressure; Brain Diseases; Disease Models, Animal; Free Radicals; Lymphatic Diseases; Male; Nitric Oxide; Rats; Rats, Wistar; Superoxide Dismutase; Systole