ABSTRACT
Background and aim: Purslane [Khurfeh] is one of the richest sources of omega3 fatty acids in plants and it has many antioxidants and minerals in its different parts. High density lipoprotein [HDL] has antioxidant effects because of Paraoxanase-1 [PON1] enzyme which attaches to HDL particles and circulates with it in blood. PON1 is responsible for hydrolysis of oxidized phospholipids. The aims of this study were investigating the Purslane effects on Paraoxanase-1 activity and lipoproteins levels, especially oxidized low density lipoprotein [OxLDL] and to compare these effects with Lovastatin
Methods: Fasting venous blood samples were obtained from patients who were referred to an internal clinic with LDL-C more than 100 mg/dl. Five ml of blood was taken before and 45 days after taking Purslane or Lovastatin. Subsequently the levels of all variables in the samples were measured using standard methods. Results were analyzed using paired t-test and t-test
Results: There was a significant decrease in serum level of cholesterol, LDL-C and OxLDL in two groups after receiving Purslane or Lovastatin [P<0.05]. ApoB was decreased only after taking Lovastatin. PON1 arylesterase activity was increased only in Purslane group following increasing of Apo A1 and HDL-C. Body mass index [BMI] and triglyceride was decreased in Purslane group [P<0.05]
Conclusion: Purslane reduces some cardiovascular risk factors through decreasing OxLDL, LDL-C, total cholesterol and triglyceride levels and increasing activity of paraoxanase-1 enzyme and HDL-C concentration. In addition, Purslane can increase ApoA1 better than Lovastatin
ABSTRACT
Background and aim: SCN1A gene encodes for neuronal voltage-gated sodium-channel ?-subunit. Mutations in this gene are the major cause of severe myoclonic epilepsy of infancy [Dravet syndrome] and generalized epilepsy with febrile seizures plus [GEFS[+]]. GEFS[+] is a heritable benign type of epilepsy associated with febrile seizures which belongs to Idiopathic Generalized Epilepsies with a marked clinical and genetic heterogeneity. The main objective of this research is screening of mutations in scn1a gene in patients affected by GEFS[+] and Idiopathic Generalized Epilepsy [IGE]
Methods: Genetic counseling was carried out with 30 patients and their family. Peripheral blood samples were collected from patients and DNA was extracted using salting out method. Standard PCR on 16[th]-26[th] exons of scn1a gene was optimized by employment of specific primers. PCR products were analyzed by SSCP in denaturant condition and sequenced in the next step
Results: Results showed a 4289c>g missense mutation in one patient affected by idiopathic generalized epilepsy. This mutation changes the alanine residue in 1430 position to glycine [A1430G]
Conclusion: More studies are needed to identify the direct role of this mutation in pathogenesis, however, heterozygotic genotype of this mutation is consistent with dominant feature of inheritance of Epilepsy