[Effects of GLAST gene knockout on phenotype and hearing in mice].

OBJECTIVE: To investigate the effects of glutamate aspartate transporter (GLAST)deletion on the normal auditory function of mice. METHODS: We hybridized GLAST+/- mice with C57BL/6J background and identified the genotypes of their offspring by agarose gel electrophoresis. 9-10-week-old mice were selected to detect the expression of GLAST protein in the cochlea by immunofluorescence staining and to verify the knockout results(n=3). The changes in weight from 7 days to 30 days after birth and the 30-day body length of male and female mice were compared(n=8). The auditory brainstem response(ABR) was used to detect the auditory threshold and the amplitude of wave I in 9-10-week-old male and female mice(n=5). RESULTS: Male GLAST-/- mice had shown significantly lower weight and body length compared to male GLAST+/+ and GLAST+/- mice(P＜0.01), and male GLAST-/- mice showed significant differences compared to GLAST+/+ from P7 to P30 statistical time. Male GLAST-/- mice exhibited a significant reduction in weight after P15 compared to male GLAST+/- mice. In contrast, no significant differences in weight and body length were observed in female GLAST-/- mice compared with female GLAST+/+ and GLAST+/- mice. There was no difference in the hearing threshold detected by ABR between the three genotypes in both male and female mice, but the amplitude of wave I in GLAST-/- mice was significantly lower than that in male GLAST+/+ mice(P＜0.01). In contrast, the amplitude of wave I in females was reduced throughout the stimulus intensity but was most significant only at high-intensity stimulation (e.g.80 dB, 90 dB) (P＜0.05). CONCLUSION: GLAST knockout affects the normal growth and development of male mice, and decreases the amplitude of wave I, but do not change the threshold, suggesting that GLAST knockout may lead to synaptic pathological changes, and there are gender differences in this effect.

The antioxidant effect of triptolide contributes to the therapy in a collagen-induced arthritis rat model.

BACKGROUND: As a chronic autoimmune disease, rheumatoid arthritis (RA) is related to oxidative stress, which may lead to the occurrence and persistence of inflammation in RA. The purpose of this study is to evaluate the potential antioxidant effect of triptolide in collagen-induced arthritis (CIA) rat model. METHODS: We examined the severity of arthritis, levels of local and systemic oxidative stress, periarticular bone erosion and weight of organs in CIA rats treated with triptolide. RESULTS: We found that triptolide decreased the paw thickness and clinical arthritis score, significantly. The mRNA expression and activity of myeloperoxidase and inducible nitric oxide synthase were remarkably decreased in the paws of the CIA rats after triptolide treatment. Triptolide significantly inhibited the levels of nitrite and nitrate in serum, as well as the urinary level of dityrosine. Triptolide treatment also markedly increased bone volume of tibia, but suppressed epiphyseal plate thickness of both femur and tibia. In addition, there was no significant difference in the weight of organs after the therapy, except decreased spleen weight. CONCLUSIONS: These results suggested that the local and systemic oxidative stress was enhanced in the CIA rats and the therapeutic dose of triptolide had a definite antioxidant effect.

[Effects of retinol acid and triiodothyronine on alleviating the impairment of cognitive function by sleep deprivation].

OBJECTIVE: To explore the effects of retinol acid (RA) and triiodothyronine (T3) on alleviating the impairment of cognitive function by sleep deprivation (SD). METHODS: Male Wistar rats were divided into 4 groups: control group (C group), sleep deprivation group (SD group), sleep deprivation + RA group (SD + RA group) and sleep deprivation + T3 group (SD + T3 group). Open field test (OFT) was used to observe the nervous behavior of the rats after SD and electrophysiological brain stereotactic method was used to test long-term potentiation (LTP) in dentate gyrus (DG) of the rats. Ng protein expression was determined by Western blot. RESULTS: Compared with the SD group, the number of crossing in OFT, the changes of amplitude of population spike (PS) and the expression of Ng protein in hippocampus were higher significantly in the SD + RA and SD + T3 groups. All of these had not significant difference comparing with the C group. CONCLUSION: RA and T3 may alleviate the restrain state of neural system after SD by augmenting the expression of Ng protein in hippocampus.

Effect of chronic noise exposure on expression of N-methyl-D-aspartic acid receptor 2B and Tau phosphorylation in hippocampus of rats.

OBJECTIVE: To study the effect of chronic noise exposure on expression of N-methyl-D-aspartic acid receptor 2B (NR2B) and tau phosphorylation in hippocampus of rats. METHODS: Twenty-four male SD rats were divided in control group and chronic noise exposure group. NR2B expression and tau phosphorylation in hippocampus of rats were detected after chronic noise exposure (100 dB SPL white noise, 4 h/d×30d) and their mechanisms underlying neuronal apoptosis in hippocampus of rats with TUNEL staining. RESULTS: The NR2B expression decreased significantly after chronic noise exposure which resulted in tau hyperphosphorylation and neural apoptosis in hippocampus of rats. Immunohistochemistry showed that the tau hyperphosphorylation was most prominent in dentate gyrus (DG) and CA1 region of rat hippocampus. CONCLUSION: The abnormality of neurotransmitter system, especially Glu and NR2B containing NMDA receptor, and tau hyperphosphorylation in hippocampus of rats, may play a role in chronic noise-induced neural apoptosis and cognition impairment.

[Effects of noise exposure on event-related potential P300 and mechanism in hippocampus of rats].

AIM: To study the effects of noise on event-related potential(ERP) and its mechanism in hippocampus in rats. METHODS: Male SD rats were divided into 2 groups: control group (CG) and noise exposure group(NG). The rats in NG were exposed to white noise 105 dB SPL for 2.5 h/d x 20 d. P300 were recorded at parietal bone in rats. The Nissl body, NMDAR2B and [Ca2+]i of neurons in hippocampus were analyzed. RESULTS: The peak latency (PL) of ERP P3a, P3 and P3b in NG were significantly longer than that in CG in the 14th and 20th exposure day. The amount of Nissl body in dentate gyrus (DG) and CA1 region and NMDAR2B in DG, CA1 and CA3 region of hippocampus of NG were significantly decreased than those of CG as well, while the concentration of Ca2+ in neurons increased markedly in NG. CONCLUSION: Decreased Nissl body and NMDAR2B and increased [Ca2+]i in hippocampus in long-term noise exposed rats might cause the change of ERP P300.

[Study of the protective effect of L-arginine on relative ischemic/reperfusion injury in myocardium of rat].

AIM: To explore the protective effect of L-arginine on isolated rat heart with ischemia/reperfusion injury. METHODS: 24 wistar rats were randomly divided into 3 groups (each 8): control group, ischemia group, L-arginine group. The myocardiac relatively ischemia/reperfusion models in vitro were set up by using weak current stimulating isolated rat hearts. During the pre-ischemia, post-ischemia 15 min and post-ischemia 30 min, the coronary fluid was collected for testing contents of MDA and activities of both CK and LDH. Cardiac functional indexes were recorded through Pclab. At the time of 5 min, 10 min, 20 min, 30 min after ischemia, the recovery of PRP, + DP/dt(max) and - DP/dt(max) were calculated. RESULTS: (1) During the reperfusion, L-arginine group achieved better recovery of cardiac function than that of the ischemia group. (2) MDA content, CK and LDH activities both in the coronary fluid and in the myocardium of L-arginine group were lower than those of the ischemia group, while SOD activities in the myocardium of L-arginine group were higher than that of the ischemia group. CONCLUSION: To some extent, L-arginine could protect the myocardium from ischemia/reperfusion injury.

[The mechanism of protection by sound conditioning from acoustic trauma].

AIM: To investigate the mechanism of protection by sound conditioning from acoustic trauma. METHODS: Sound conditioning experimental model of animals was established. The expression of CaM, HSP70 and F-actin in hair cells were examined with the method of immunohistochemistry. Free calcium concentration in hair cells was observed by LSCM at the same time. Quantitative investigation was devised to assess the changes of F-actin, CaM, HSP70 and intracellular calcium concentration in hair cells. RESULTS: The expression of CaM, HSP70 and F-actin all showed an increased trend after noise exposure. HSP70 and F-actin expressed significantly more in group CH than that expressed in group H. Compared with group H, the expression of CaM showed an increased trend in group CH. Elevation of intracellular calcium concentration could be resulted from noise exposure. The calcium concentration in group H was significantly higher than that in group C and group CH. CONCLUSION: A suitable sound conditioning can make the auditory system of guinea pig more resistant to noise trauma. The strengthened cytoskeleton system and the intracellular calcium homeostasis play a critical role in the protective mechanism of sound conditioning.