33 research outputs found
Suberoylanilide hydroxamic acid attenuates cognitive impairment in offspring caused by maternal surgery during mid-pregnancy.
No full textSome pregnant women have to experience non-obstetric surgery during pregnancy under general anesthesia. Our previous studies showed that maternal exposure to sevoflurane, isoflurane, propofol, and ketamine causes cognitive deficits in offspring. Histone acetylation has been implicated in synaptic plasticity. Propofol is commonly used in non-obstetric procedures on pregnant women. Previous studies in our laboratory showed that maternal propofol exposure in pregnancy impairs learning and memory in offspring by disturbing histone acetylation. The present study aims to investigate whether HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) could attenuate learning and memory deficits in offspring caused by maternal surgery under propofol anesthesia during mid-pregnancy. Maternal rats were exposed to propofol or underwent abdominal surgery under propofol anesthesia during middle pregnancy. The learning and memory abilities of the offspring rats were assessed using the Morris water maze (MWM) test. The protein levels of histone deacetylase 2 (HDAC2), phosphorylated cAMP response-element binding (p-CREB), brain-derived neurotrophic factor (BDNF), and phosphorylated tyrosine kinase B (p-TrkB) in the hippocampus of the offspring rats were evaluated by immunofluorescence staining and western blot. Hippocampal neuroapoptosis was detected by TUNEL staining. Our results showed that maternal propofol exposure during middle pregnancy impaired the water-maze learning and memory of the offspring rats, increased the protein level of HDAC2 and reduced the protein levels of p-CREB, BDNF and p-TrkB in the hippocampus of the offspring, and such effects were exacerbated by surgery. SAHA alleviated the cognitive dysfunction and rescued the changes in the protein levels of p-CREB, BDNF and p-TrkB induced by maternal propofol exposure alone or maternal propofol exposure plus surgery. Therefore, SAHA could be a potential and promising agent for treating the learning and memory deficits in offspring caused by maternal nonobstetric surgery under propofol anesthesia
Propofol exposure during early gestation impairs learning and memory in rat offspring by inhibiting the acetylation of histone
No full textRecovery of Iron-, Titanium-Bearing Constituents from Bauxite Ore Residue via Magnetic Separation Followed by Sulfuric Acid Leaching
No full textThe physical characteristics of rats’ offspring.
No full textA) Body weight of offspring rats; B) Total litter size in each group; C) Survival rate of offspring rats (defined as the ratio of rat offspring that survived over P30 day); D) Gender composition in each group. There was no significant difference in these indexes among the control, propofol and surgery groups. The data are expressed as means ± SD.</p
Propofol anesthesia or with surgery enhanced the expression of HDAC2 and SAHA reversed the enhancement.
No full textA) Immunofluorescence images for the distribution of HDAC2-positive cells and neun neurobiomarkers in the hippocampus. (green represents HDAC2 and red represents Neun). B) Western blotting images for HDAC2 protein expression in the hippocampus. C) There was a significant increase in the protein level of HDAC2, especially in the propofol anesthesia plus surgery. (*p p < 0.05 vs. DMSO). The data are presented as means ± SD. n = 6 per group; female:male = 3:3.</p
Propofol anesthesia or with surgery decreased the expression of BDNF and p-TrkB, but SAHA reversed the reduction.
No full textA) Western blotting bands of BDNF. B) Western blotting bands of p-TrkB. C) BDNF protein levels (BDNF protein %DMSO Control): propofol exposure and surgery significantly decreased the expression level of BDNF. Compared with Control+DMSO group, (*p p p p = 0.05 vs. Surgery+SAHA). D) p-TrkB protein levels in rat offspring’s hippocampus: propofol anesthesia decreased p-TrkB protein levels significantly. While propofol anesthesia plus surgery, the levels of p-TrkB protein decreased much more significantly. Compared with Control+DMSO group, (*p p p p Note: the data are presented as the mean ± SD. n = 6 in each group, female: male = 3:3.</p
Propofol anesthesia or with surgery decreased the expression of p-CREB and SAHA reversed the reduction.
No full textA) Immunofluorescence image for the distributive expression of p-CREB. B) Western blotting images for p-CREB protein. C) There was no difference between the Control+SAHA and the Control+DMSO. The protein levels of p-CREB were downregulated expression in the Propofol+DMSO (*p p p p < 0.001 vs. DMSO group). The data are presented as means ± SD. n = 6 per group, female: male = 3:3.</p
The flow chart of experimental protocols.
No full textA) The flow chart of the experimental protocols and distribution of offspring rats across different studies; B) The time-line of experimental paradigms. The number in brackets represents the number of animals. F, female; M, male; SAHA, HDAC2 inhibitor vorinostat; DMSO, dimethyl sulfoxide; IF, Immunofluorescence; TUNEL, terminal deoxynucleotidyl transferase mediated nick end labeling; E14, pregnant rats at gestational day 14; P0, postnatal day 0; ip, intraperitoneally.</p
S1 Raw images -
No full textSome pregnant women have to experience non-obstetric surgery during pregnancy under general anesthesia. Our previous studies showed that maternal exposure to sevoflurane, isoflurane, propofol, and ketamine causes cognitive deficits in offspring. Histone acetylation has been implicated in synaptic plasticity. Propofol is commonly used in non-obstetric procedures on pregnant women. Previous studies in our laboratory showed that maternal propofol exposure in pregnancy impairs learning and memory in offspring by disturbing histone acetylation. The present study aims to investigate whether HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) could attenuate learning and memory deficits in offspring caused by maternal surgery under propofol anesthesia during mid-pregnancy. Maternal rats were exposed to propofol or underwent abdominal surgery under propofol anesthesia during middle pregnancy. The learning and memory abilities of the offspring rats were assessed using the Morris water maze (MWM) test. The protein levels of histone deacetylase 2 (HDAC2), phosphorylated cAMP response-element binding (p-CREB), brain-derived neurotrophic factor (BDNF), and phosphorylated tyrosine kinase B (p-TrkB) in the hippocampus of the offspring rats were evaluated by immunofluorescence staining and western blot. Hippocampal neuroapoptosis was detected by TUNEL staining. Our results showed that maternal propofol exposure during middle pregnancy impaired the water-maze learning and memory of the offspring rats, increased the protein level of HDAC2 and reduced the protein levels of p-CREB, BDNF and p-TrkB in the hippocampus of the offspring, and such effects were exacerbated by surgery. SAHA alleviated the cognitive dysfunction and rescued the changes in the protein levels of p-CREB, BDNF and p-TrkB induced by maternal propofol exposure alone or maternal propofol exposure plus surgery. Therefore, SAHA could be a potential and promising agent for treating the learning and memory deficits in offspring caused by maternal nonobstetric surgery under propofol anesthesia.</div
KIF17 mediates the learning and memory impairment in offspring induced by maternal exposure to propofol during middle pregnancy
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