Sleep deprivation can be described as inadequate quantity or quality of sleep characterized by insufficient sleep duration, delayed sleep onset, and occurrence of napping episodes during the day. Sleep deprivation in animals and obstructive sleep apnea syndrome in human was reported to be associated with increased oxidative stress. Glycyrrizha glabra (licorice) is a medicinal plant known to be a highly efficacious medicinal herb with several pharmacological effects. Hence, the aim of this study was to demonstrate whether or not licorice root extract will regulate the imbalance between the reactive oxygen species and production of antioxidant enzymes in the brain of sleep deprived rats. Twenty - five 6-week-old male Wistar rats were randomly divided into five groups to undergo sleep deprivation and recovery for 5 days each. Group I (Control): Group II: sleep deprivation (SD); Group III: sleep deprivation and recovery (SD+SR) all received distill water (10ml/kg) orally; Group IV: sleep deprivation and licorice (SD+Lic), Group V: sleep deprivation, recovery with licorice (SD+SR+Lic) both received licorice (150mg/kg) orally once daily. MDA concentration among rats in Groups II (51%), III (46.7%) and IV (31.3%) were significantly higher when compared with control. Rats in Group III (20.5%), Group IV (24.6%) and Group V (30.8%) showed increased significant change in GSH concentration when compared with Group II. The concentration of CAT among rats in Group II was significantly lower than those rats in Group III (43.8%), Group IV (53.8%) and Group V (72.9%). These results clearly show that sleep deprivation significantly affects the oxidative status of rats. In conclusion, licorice root extract has ameliorative effect on the imbalance between the reactive oxygen species and production of antioxidant enzymes in the brain of sleep deprived rats.
Sleep ; Sleep Deprivation ; Oxidative Stress, Rats

OBJECTIVE: To study the effects and mechanisms of curcumin alleviating oxidative stress induced by overtraining and inhibiting renal apoptosis in rats. METHODS: Male Wistar rats of 7 weeks old were divided into control group (C group, 12), overtraining group (OM group, 11), curcumin + overtraining group (COM group, 14). Group C did not undergo any exercise intervention. Rats in OM group and COM group underwent 8-week incremental load swimming training. During the training, the COM group was treated with curcumin at the dose of 200 mg/(kg·d) in the volume as 5 ml/kg by intragastric administration, and the other groups was treated with an equal volume of 0.5% carboxymethylcellulose. Twenty-four hours after the last training, renal histopathological changes were observed by light microscopy, related biochemical indicators in blood and renal tissue were detected. RESULTS: The results showed that after 8 weeks of incremental load swimming training, the renal tissue structure of group C was normal under light microscope; histopathological changes were observed in OM group; COM group was significantly relieved compared with OM group. Compared with group C, serum levels of corticosterone (Cor), creatinine (Cr) and blood urea nitrogen (BUN) in OM group were increased (<0.01), serum level of testosterone (T) was lower (<0.01); the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) was not changed significantly (>0.05), while the expression of heme oxygenase-1 (HO-1) was decreased (<0.05), total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity were decreased (<0.01), malondialdehyde (MDA) concentration was increased (<0.01); the renal apoptosis was increased (<0.01), the expression of anti-apoptotic B cell lymphoma-2 protein (Bcl-2) was decreased (<0.01), and the expression of proapoptotic Bcl-2 associated X protein (Bax) was increased (<0.01). Compared with the OM group, Cor level was decreased (<0.01) in the COM group, T level was increased (<0.01), Cr and BUN levels were lower (<0.05); the expression of Nrf2 and HO-1 were increased (<0.05), T-AOC and SOD activity were increased (<0.01), MDA concentration was decreased (<0.05); the renal apoptosis was decreased (<0.05), the expression of Bcl-2 was increased (<0.05), and the expression of Bax was decreased (<0.01). The trend of testosterone/corticosterone ratio between groups was consistent with testosterone change, and the change trend of Bcl-2/Bax ratio was consistent with the change of Bcl-2. CONCLUSIONS The 8-week incremental load swimming training triggered excessive training in rats, aggravated oxidative stress and accelerated renal apoptosis, leading to pathological changes and dysfunction of kidney. Curcumin can up-regulate expression of Nrf2 and HO-1, effectively alleviates oxidative stress induced by overtraining, thereby increasing Bcl-2 expression, decreasing Bax expression, inhibiting renal apoptosis and protecting renal tissue structure and function properly.
Animals ; Apoptosis ; Curcumin ; Kidney ; Male ; Oxidative Stress ; Rats ; Rats, Wistar

OBJECTIVES: In this study we investigated the probable protective effects of thymoquinone on amikacin-induced ototoxicity in rats. METHODS: Thirty-two healthy rats were divided into four groups (amikacin, amikacin+thymoquinone, thymoquinone, and no treatment). Thymoquinone was fed to the rats via oral gavage in a dose of 40 mg/kg/day throughout the study period of 14 days. Amikacin was given by the intramuscular route in a dose of 600 mg/kg/day. Audiological assessment was conducted by the distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) tests, administered to all rats at the beginning of the study, and also on days 7 and 15. Biochemical parameters were calculated at the termination of the study to evaluate the oxidative status. RESULTS: There were significant decreases in DPOAE values and significant increases in ABR thresholds of the amikacin group on days 7 and 15, as compared to the amikacin+thymoquinone group. While ABR thresholds of the amikacin group increased significantly on days 7 and 15 as compared to their initial values, there were no significant differences between the initial and the 7th and 15th day values of ABR thresholds in the amikacin+thymoquinone group. Total oxidant status and oxidative stress index values of the amikacin+thymoquinone group were significantly lower than those of the amikacin group. Total antioxidant status values of the amikacin+thymoquinone group were significantly higher than those of the amikacin group. CONCLUSION: Our study has demonstrated that the ototoxic effect brought forth by amikacin could be overcome with the concurrent use of thymoquinone.
Amikacin ; Animals ; Evoked Potentials, Auditory, Brain Stem ; Oxidative Stress ; Rats*

Animals ; Models, Neurological ; Oxidative Stress ; PC12 Cells ; Rats

In this study, we investigated the protective action of glucuronopyranoside flavonoids (QGC, AGC, LGC) on gastritis in rats. QGC, AGC and omeprazole decreased the gastric volume significantly, and each ID50 was 0.75, 0.54 and 8.5 mg/kg, respectively, thus the order of potency was AGC, QGC and omeprazole. They also decreased acid output, and each ID50 was 7.81, 0.58 and 6.71 mg/kg, respectively, thus the order of potency was AGC, omeprazole and QGC. They inhibited gastritis induced by indomethacin, and it recovered significantly by increasing the GSH levels in gastritis. The gastric MPO activity in the gastritis group increased more than in the normal group. QGC, LGC, or AGC administration reduced moderately the MPO activity in a dose-dependent manner. This study demonstrated that AGC, QGC, or LGC showed potent efficacy on the gastritis, by preventing oxidative stress. These results suggest that QGC, AGC, or LGC have gastroprotective effect in rats.
Animals ; Flavonoids* ; Gastritis ; Indomethacin ; Lipid Peroxidation ; Omeprazole ; Oxidative Stress ; Rats*

Animals ; Calreticulin ; metabolism ; Male ; Muscle, Skeletal ; metabolism ; Oxidative Stress ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley

BACKGROUND/AIMS: The role of uncoupling protein-2 (UCP2) in the liver is currently unclear. Emerging evidence suggests a relationship between UCP2 and oxidative stress. In the present study, we tested the hypothesis that UCP2 expression in the liver might change during warm ischemia-reperfusion (I/R) according to oxidative stress. METHODS: Wistar rats were subjected to 40 (short ischemia) or 90 (long ischemia) minutes of partial lobar ischemia followed by 4 hours of reperfusion. UCP2 expression in the ischemic and nonischemic lobes was assessed using reverse transcription-polymerase chain reaction and immunohistochemistry. Malondialdehyde concentrations in the liver tissue were also compared. RESULTS: Malondialdehyde concentrations in the ischemic lobes were significantly higher in the long ischemia group. In the ischemic lobes of the short ischemia group, UCP2 protein expression was induced in hepatocytes, which did not express the protein prior to treatment, and the expression levels were higher than in the long ischemia group. The intralobular distribution of UCP2 seemed to correlate inversely with that of the necrotic area. UCP2 expression was observed, even in nonischemic lobes with similar intralobular heterogeneity. CONCLUSIONS: UCP2 was induced in hepatocytes after warm I/R. Although the primitive role of UCP2 expression may be cytoprotective in nature, its actual protective effect in hepatic I/R may be minimal
Animals ; Hepatocytes ; Immunohistochemistry ; Ion Channels ; Ischemia ; Liver ; Malondialdehyde ; Mitochondrial Proteins ; Oxidative Stress ; Rats ; Rats, Wistar ; Reperfusion

Inorganic arsenic (iAs) is a toxic metalloid found ubiquitously in the environment. In humans, exposure to iAs can result in toxicity and cause toxicological manifestations. Arsenic trioxide (As2O3) has been used in the treatment for acute promyelocytic leukemia. The kidney is the critical target organ of trivalent inorganic As (iAsIII) toxicity. We examine if oral administration of astaxanthin (AST) has protective effects on nephrotoxicity and oxidative stress induced by As2O3 exposure (via intraperitoneal injection) in rats. Markers of renal function, histopathological changes, Na+-K+ ATPase, sulfydryl, oxidative stress, and As accumulation in kidneys were evaluated as indicators of As2O3 exposure. AST showed a significant protective effect against As2O3-induced nephrotoxicity. These results suggest that the mechanisms of action, by which AST reduces nephrotoxicity, may include antioxidant protection against oxidative injury and reduction of As accumulation. These findings might be of therapeutic benefit in humans or animals suffering from exposure to iAsIII from natural sources or cancer therapy.
Adenosine Triphosphatases ; Administration, Oral ; Animals ; Arsenic ; Humans ; Kidney ; Leukemia, Promyelocytic, Acute ; Oxidative Stress ; Rats ; Rats, Wistar*

Animals ; Brain Injuries ; metabolism ; therapy ; Cytokines ; metabolism ; Hyperbaric Oxygenation ; Male ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To explore the effect of chronic intermittent hypoxia (CIH) on liver injury and to examine the expression of liver CXC chemokine ligand-10 (CXCL10) in the rats, and to explore the effect of N-acetylcysteine (NAC).
 METHODS: A total of 21 male SD rats were randomly divided into a control group, a CIH group and a CIH+NAC group (n=7 in each group). The control group exposed to normal gaseous environment, the other 2 groups were exposed to CIH for 5 weeks (8 h/d); the control group and the CIH group were given daily saline lavage, the CIH+NAC group daily received NAC solution. After the end of 5 weeks, the rats were killed, and the MDA content and SOD activity in rat liver tissues were detected. The liver sections were stained with hematoxylin-eosin (HE) and the liver pathology was observed. The expression of CXCL10 in the liver tissues was detected by immunohistochemical method.
 RESULTS: Compared with the control group, the MDA levels in rat liver tissues were increased (P<0.05), and the SOD levels were decreased (P<0.05) in the CIH group and the CIH+NAC group. Compared with the CIH group, the SOD levels in the rat liver tissues were increased (P<0.05), and the MDA levels were decreased in the CIH+NAC group. Compared with the control group, the hepatic steatosis and inflammatory reactions were more severe in the CIH group and the CIH+NAC group (both P<0.01). Compared with the CIH group, the hepatic steatosis and inflammatory reactions were reduced in the CIH+NAC group (P<0.05). The liver damage in the CIH+NAC group was less than that in the CIH group (P<0.05). Compared with the control group, the CXCL10 expression in the CIH group and the CIH+NAC group was increased (both P<0.01). The CXCL10 expression in the CIH+NAC group was down-regulated compared with that in the CIH group (P<0.01).
 CONCLUSION CIH can lead to liver injury and induce CXCL10 expression in rat liver tissues. The NAC can alleviate rat liver oxidative stress and inflammation caused by CIH, and in turn to improve the liver injury in rats.
Acetylcysteine ; Animals ; Chemokine CXCL10 ; Fatty Liver ; Hypoxia ; Inflammation ; Male ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley