Lead exposure through gestation-only caused long-term learning/memory deficits in young adult offspring.

Numerous observations in clinical and preclinical studies indicate that the developing brain is particular sensitive to lead (Pb)'s pernicious effects. However, the effect of gestation-only Pb exposure on cognitive functions at maturation has not been studied. We investigated the potential effects of three levels of Pb exposure (low, middle, and high Pb: 0.03%, 0.09%, and 0.27% of lead acetate-containing diets) at the gestational period on the spatial memory of young adult offspring by Morris water maze spatial learning and fixed location/visible platform tasks. Our results revealed that three levels of Pb exposure significantly impaired memory retrieval in male offspring, but only female offspring at low levels of Pb exposure showed impairment of memory retrieval. These impairments were not due to the gross disturbances in motor performance and in vision because these animals performed the fixed location/visible platform task as well as controls, indicating that the specific aspects of spatial learning/memory were impaired. These results suggest that exposure to Pb during the gestational period is sufficient to cause long-term learning/memory deficits in young adult offspring.

The stress experience dependent long-term depression disassociated with stress effect on spatial memory task.

Behavioral stress can either block or facilitate memory and affect the induction of long-term potentiation (LTP) and long-term depression (LTD). However, the relevance of the stress experience-dependent long-term depression (SLTD) to spatial memory task is unknown. Here we have investigated the effects of acute and sub-acute elevated platform (EP) and foot shock (FS) stress on LTD induction in CA1 region of the hippocampus of anesthetized rats and spatial memory in Morris water maze. We found that LTD was facilitated by acute EP stress, but not by sub-acute EP stress that may be due to the fast adaptation of the animals to this naturalistic mild stress. However, FS stress, an inadaptable strong stress, facilitated LTD induction both in acute and sub-acute treatment. In addition, with the same stress protocols, acute EP stress impaired spatial memory but the sub-acute EP stressed animals performed the spatial memory task as well as the controls, may due to the same reason of adaptation. However, acute FS stress slightly impaired learning but sub-acute FS even enhanced memory retrieval. Our results showed that SLTD was disassociated with the effect of stress on memory task but might be related to stress experience-dependent form of aberrant memory.

Effect of caffeic acid phenethyl ester on proliferation and apoptosis of hepatic stellate cells in vitro.

AIM: To investigate the role of nuclear factor-kappaB (NF-kappaB) inhibitor caffeic acid phenethy1 ester (CAPE) in the proliferation, collagen synthesis and apoptosis of hepatic stellate cells (HSCs) of rats. METHODS: The HSCs from rats were isolated and cultured in Dulbecco's Modified Eagle's Medium (DMEM) and treated with CAPE. The proliferation and collagen synthesis of HSCs were determined by (3)H-TdR and (3)H-proline incorporation respectively, and the expression of type I, III procollagen genes was further explored by in situ hybridization. Apoptosis cell indices (AIs) were examined using terminal deoxynucleotidyl transferase- mediated DIG-dUTP nick end labeling (TUNEL). RESULTS: In activated HSC in culture, CAPE significantly inhibited (3)H-TdR and (3)H-proline incorporation by HSCs at concentrations of 5 micromol/L and 10 micromol/L respectively. CAPE also reduced the type I procollagen gene expression (P<0.05) at higher concentration. Apoptosis of HSC was induced by CAPE and the AIs were time-and dose-dependently increased from 2.82+/-0.73 % to 7.66+/-1.25 % at 12 h (P<0.01) and from 3.15+/-0.88 % to 10.61+/-2.88 % at 24 h (P<0.01). CONCLUSION: CAPE inhibits proliferation and collagen synthesis of HSC at lower concentration and induces HSC apoptosis at higher concentration.

[Luteolin inhibits proliferation and collagen synthesis of hepatic stellate cells].

OBJECTIVE: To investigate the effect of luteolin on the proliferation and collagen expression of hepatic stellate cells. METHODS: The effect of luteolin on proliferation and collagen synthesis of hepatic stellate cells isolated from the liver of Wistar rats were determined by (3)H-TdR and (3)H-Pro, and procollagen gene expression was also detected by DIG-labeled gene probe and in situ hybridization. RESULTS: The proliferation and collagen synthesis were significantly and dose-dependently inhibited by luteolin when the concentrations reached 10 micromol/L and 20 micromol/L respectively (t=2.542, P<0.05; t=3.650, P<0.01). The type I, III procollagen mRNA expression was decreased by 25 micromol/L luteolin, in which the type I procollagen mRNA was reduced with statistical significance (x(2)=6.850, P<0.01). CONCLUSIONS: Luteolin inhibits the proliferation and collagen expression of hepatic stellate cells in vitro. It may have a preventive or therapeutic role in liver fibrosis.

Propofol facilitates the development of long-term depression (LTD) and impairs the maintenance of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats.

Memory is sensitive to the short-acting anesthetic (2,6-diisopropylphenol) propofol, but the underlying mechanism is little known. Here, we have examined the effects of propofol on synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats. We found that low dose of propofol (20 mg/kg, i.p.) did not affect the basal transmission, but enhanced prominently the development of long-term depression (LTD) and impaired the maintenance of long-term potentiation (LTP). The impairment of LTP maintenance and enhancement of LTD development may contribute to propofol-induced deficits in memory following propofol anesthesia.

[Zymography identification of the matrix metalloproteinases synthesized by cultured hepatic stellate cells].

AIM: To establish a method for identification of the activities of matrix metalloproteinases (MMPs) synthesized by cultured hepatic stellate cells (HSC). METHODS: SDS-gelatin polyacrylamide gels electrophoresis was used for the identification of MMPs synthesized by cultured HSC. RESULTS: MMP-2 and MMP-9 in culture medium and HSC were sensitively identified, and MMP-2 activity was higher than MMP-9 in culture medium, the changes of MMPs in culture medium and HSC were also observed after 24h medicine treatment. CONCLUSION: Zymography is suitable for the studies on the role of HSC in the regulation of extracellular matrix turnover.