The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel dis- ease in rats. Naringin （20, 40 and 80 mg/kg） was given orally for 7 days to Wistar rats before induction...The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel dis- ease in rats. Naringin （20, 40 and 80 mg/kg） was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4% （v/v） acetic acid solution. The degree of colonic mucosal damage was analyzed by examining mucosal damage, ulcer area, ulcer index and stool consistency. Intrarectal administration of 4% acetic acid resulted in significant modulation of serum alkaline phosphatase, lactate dehydrogenase, superoxide dismutase （SOD）, glutathione （GSH）, malondialdehyde （MDA） and myeloperoxidase （MPO） content along with colonic nitric oxide （NO）, xanthine oxidase （XO） level and protein carbonyl content in the colonic tissue as well as in blood. Naringin （40 and 80 mg/kg） exerted a dose dependent （P 〈 0.05） ameliorative effect, as it significantly increased hematological parameter as well as colonic SOD and GSH. There was a significant （P 〈 0.05） and dose dependant inhibition of macroscopical score, ulcer area along with colonic MDA, MPO activity by the 7 days of pretreatment of naringin （40 and 80 mg/kg）. Biochemical studies revealed a significant （P 〈 0.05） dose dependant inhibition in serum alkaline phosphatase （ALP） and lactate dehydrogenase （LDH） levels by pretreatment of naringin. Increased levels of colonic NO, XO, protein carbonyl content and DNA damage were also sig- nificantly decreased by naringin pretreatment. The findings of the present investigation propose that naringin has an anti-inflammatory, anti-oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the production and expression of oxidative mediators such as MDA, MPO, NO and XO, thus reducing DNA damage.展开更多
Background: Attention-deficit hyperactivity disorder (ADHD) is a widespread and debilitating disorder with relatively high prevalence in Saudi Arabia. Neuropsychological and radiological investigations have revealed t...Background: Attention-deficit hyperactivity disorder (ADHD) is a widespread and debilitating disorder with relatively high prevalence in Saudi Arabia. Neuropsychological and radiological investigations have revealed that there are some differences in the components of the brain regions in children with and without ADHD. In this study we have performed whole exome sequencing (WES) in four non-familial cases of ADHD from Makkah Region to identify the genetic polymorphisms associated with the disease in our Saudi population. Methods: Exome sequencing was carried out using Ion Proton with AmpliSeq Exome library methods, and the data were analysed by Ion Reporter 5.6 software. Results: A total of 33 variants were identified from 222 genes selected from the GWAS catalogue for ADHD associated genes. However, the SNPs we identified in these genes were not reported to be associated with ADHD in previous studies. We have identified 2 novel missense variants;one in c.3451G > T;p. (Ala1151Ser) in ITGA1 gene and another is c.988G > A;p. (Ala330Thr) in SPATA13 genes. The variants rs928661, rs11150370 and rs386792899 were the only three variants that appeared on all the 4 patients studied. Six missense variants, rs16841277, rs2228209, rs2230283, rs3741883, rs1716 and rs2272606, were found in 3 different patients, respectively. However, the three documented variants are rs13166360 with bipolar disorder, rs920829 with neuropathic pain, and rs6558702 with schizophrenia. Conclusion: We have identified 2 novel variants in ADHD children. SIFT score of all variants indicates that these substitutions have damaging effects on the protein function. Further screening studies are recommended for confirmation.展开更多
文摘The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel dis- ease in rats. Naringin （20, 40 and 80 mg/kg） was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4% （v/v） acetic acid solution. The degree of colonic mucosal damage was analyzed by examining mucosal damage, ulcer area, ulcer index and stool consistency. Intrarectal administration of 4% acetic acid resulted in significant modulation of serum alkaline phosphatase, lactate dehydrogenase, superoxide dismutase （SOD）, glutathione （GSH）, malondialdehyde （MDA） and myeloperoxidase （MPO） content along with colonic nitric oxide （NO）, xanthine oxidase （XO） level and protein carbonyl content in the colonic tissue as well as in blood. Naringin （40 and 80 mg/kg） exerted a dose dependent （P 〈 0.05） ameliorative effect, as it significantly increased hematological parameter as well as colonic SOD and GSH. There was a significant （P 〈 0.05） and dose dependant inhibition of macroscopical score, ulcer area along with colonic MDA, MPO activity by the 7 days of pretreatment of naringin （40 and 80 mg/kg）. Biochemical studies revealed a significant （P 〈 0.05） dose dependant inhibition in serum alkaline phosphatase （ALP） and lactate dehydrogenase （LDH） levels by pretreatment of naringin. Increased levels of colonic NO, XO, protein carbonyl content and DNA damage were also sig- nificantly decreased by naringin pretreatment. The findings of the present investigation propose that naringin has an anti-inflammatory, anti-oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the production and expression of oxidative mediators such as MDA, MPO, NO and XO, thus reducing DNA damage.
文摘Background: Attention-deficit hyperactivity disorder (ADHD) is a widespread and debilitating disorder with relatively high prevalence in Saudi Arabia. Neuropsychological and radiological investigations have revealed that there are some differences in the components of the brain regions in children with and without ADHD. In this study we have performed whole exome sequencing (WES) in four non-familial cases of ADHD from Makkah Region to identify the genetic polymorphisms associated with the disease in our Saudi population. Methods: Exome sequencing was carried out using Ion Proton with AmpliSeq Exome library methods, and the data were analysed by Ion Reporter 5.6 software. Results: A total of 33 variants were identified from 222 genes selected from the GWAS catalogue for ADHD associated genes. However, the SNPs we identified in these genes were not reported to be associated with ADHD in previous studies. We have identified 2 novel missense variants;one in c.3451G > T;p. (Ala1151Ser) in ITGA1 gene and another is c.988G > A;p. (Ala330Thr) in SPATA13 genes. The variants rs928661, rs11150370 and rs386792899 were the only three variants that appeared on all the 4 patients studied. Six missense variants, rs16841277, rs2228209, rs2230283, rs3741883, rs1716 and rs2272606, were found in 3 different patients, respectively. However, the three documented variants are rs13166360 with bipolar disorder, rs920829 with neuropathic pain, and rs6558702 with schizophrenia. Conclusion: We have identified 2 novel variants in ADHD children. SIFT score of all variants indicates that these substitutions have damaging effects on the protein function. Further screening studies are recommended for confirmation.
