ABSTRACT
Objective To study the effect of extracts of Smilax china L. on inhibition the experimentally induced benign prostatic hyperplasia ( BPH) , and screen the effective fraction. Methods The BPH model was built on the castrated rats by subcutaneous injection of testosterone propionate. Male rats were randomly divided into eight groups ( n=6 ):sham operation, model control, petroleum ether fraction, acetic ether fraction, n-butyl alcohol fraction, water fraction, macroporous resin fraction ( FMR) , and total extracts group. The rats were treated with testosterone propionate by subcutaneous injection for consecutive 3 weeks. Meanwhile, rats were orally administrated with the six extract fractions of S. china L. After the last administration, serum was separated for the determination of prostatic acid phosphatase ( PACP ) , prostate was weighed and histopathological examination was carried out to evaluate the inhibitory effect of S. china L. against BPH. Results All of the six fractions from S. china L. could inhibit BPH, and the n-butanol fraction, water fraction and FMR showed better inhibitory effect, which significantly decreased the prostatic index by 52. 80%, 50. 93% and 67. 70%, respectively, remarkably reduced serum PACP, and notably improved the prostate gland morphology compared with the model group. Among the three fractions, FMR showed the strongest effect against BPH. Conclusion S. china L. ameliorates the experimentally prostatic hyperplasia, and FMR showes the best effect, which might be the bioactive components against BPH.
ABSTRACT
Growing genetic evidence is converging in favor of common pathogenic mechanisms for autism spectrum disorders (ASD), intellectual disability (ID or mental retardation) and schizophrenia (SCZ), three neurodevelopmental disorders affecting cognition and behavior. Copy number variations and deleterious mutations in synaptic organizing proteins including NRXN1 have been associated with these neurodevelopmental disorders, but no such associations have been reported for NRXN2 or NRXN3. From resequencing the three neurexin genes in individuals affected by ASD (n = 142), SCZ (n = 143) or non-syndromic ID (n = 94), we identified a truncating mutation in NRXN2 in a patient with ASD inherited from a father with severe language delay and family history of SCZ. We also identified a de novo truncating mutation in NRXN1 in a patient with SCZ, and other potential pathogenic ASD mutations. These truncating mutations result in proteins that fail to promote synaptic differentiation in neuron coculture and fail to bind either of the established postsynaptic binding partners LRRTM2 or NLGN2 in cell binding assays. Our findings link NRXN2 disruption to the pathogenesis of ASD for the first time and further strengthen the involvement of NRXN1 in SCZ, supporting the notion of a common genetic mechanism in these disorders.
