Mesalamine (5-aminosalicylic acid or 5-ASA or Mesalazine) is the first-line anti-inflammatory agent recommended for the treatment of Ulcerative colitis (UC) and Crohn's disease (CD) (collectively termed inflammatory bowel disease -IBD) [1]. Mesalamine acts topically on the colonic mucosa but when orally administered, it is extensively and rapidly absorbed in the small intestine, leading to little localization of Mesalamine in the colon and hence, low efficiency with significant systemic side effects [2]. Various Mesalamine drug delivery systems are developed to deliver varying amounts of drug to the intended site of action, which may have an effect on the bioavailability and therapeutic efficacy. The available oral 5-ASA products are developed using mainly three types of drug delivery systems: a pro-drug concept, enteric or delayed release coating, and/or prolonged release formulations [3]. pH dependent delayed-release formulations start the drug release when the pH of gastric environment is above pH 6-7.
Mesalamine (5-aminosalicylic acid or 5-ASA or Mesalazine) is the first-line anti-inflammatory agent recommended for the treatment of active symptoms, induction of remission and maintenance of remission in patients with mild-to-moderate ulcerative colitis [1]. Mesalamine acts topically on the colonic mucosa but when orally administered, it is extensively and rapidly absorbed in the small intestine, leading to little localization of Mesalamine in the colon and hence, low efficiency with significant systemic side effects [2].Consequently, three methods have been commonly used for targeting of Mesalamine to the colon: a pro-drug concept, enteric coating, and/or prolonged release of the drug through semi permeable membrane [3].The recommended daily dose of Mesalamine may reach 4.8 g in acute attack and 2.4 g in maintenance of remission in divided doses. Therefore, multiple daily dosing up to 12 tablets or capsules per day are required because of the low dosage strength of most currently commercially available Mesalamine formulations. Reduced patient compliance and disease control are the results of these inconveniences of frequent daily dosing and the number of tablets or capsules required per day [4]. Additionally, many traditional delayed-release formulations that lack any means for prolonging Mesalamine release are characterized by the
Objective: The objective of the present study was to explore the in vitro antioxidant and effect of hydroalcoholic extract of Arthrospira platensis (ASP) against sodium fluoride (NaF)-induced toxic effects on soft tissues (heart, liver, and kidney).Methods: In vitro antioxidant activity was assessed using 1,1-diphenyl-2-picrylhydrazyl radical scavenging, 2,2’-azino-bis(3-ethylbenzothiazoline- 6-sulphonic acid) radical scavenging, metal chelation, total antioxidant and reducing power assays, and total flavonoid and phenol content. In this study, 36 male Wistar albino rats were divided into six groups of six animals each. Animals were served as Group I - normal control, Group II - toxic control, and Groups III, IV, and V - treatment groups, which received hydroalcoholic extract of ASP at doses of 100, 200, and 400 mg/kg body weight (p.o), respectively. Group VI served as plant control received hydroalcoholic extract of ASP at a dose of 400 mg/kg body weight (p.o). All groups except Groups I and VI received NaF (100 ppm) through drinking water for 30 days.Results: Results showed that intoxication of NaF caused significant elevation of serum biomarkers of the heart, liver, and kidney and altered tissue oxidative stress markers’ levels. Administration of hydroalcoholic extract of ASP significantly normalized elevated serum levels of heart (p<0.001), liver (p<0.001, p<0.05), and kidney biomarkers (p<0.001). Decrease in lipid peroxidation and increase in reduced glutathione and catalase enzyme levels in a dose-dependent manner were observed in soft tissues (p<0.001, p<0.01, and p<0.05).Conclusion: The study revealed that ASP has good antioxidant and mitigative action against NaF intoxication on soft tissues.
Glimepiride [1][2][3][4] is the only third generation sulphonyl urea, which lowers the blood glucose level in the healthy subjects as well as in patients with type II diabetes. After oral administration, Glimepiride is completely (100%) absorbed from the GI tract. Studies with single oral doses in normal subjects and with multiple oral doses in patients with type II diabetes have shown significant absorption of Glimepiride within 1 hour after administration and peak drug levels (C max ) at 2 to 3 hours. Due to its low biological half life, it requires frequent administration to maintain plasma concentration. This leads fluctuations in plasma
The objective of the present study was to explore the alleviatory effects of hydroalcoholic extract of Brassica oleracea var. botrytis (BOB) leaves against sodium fluoride (NaF)-induced cardiotoxicity. Animals served as group I (normal control), group II (toxic control) and groups III-V (treatment groups) received extract at doses of 100, 200 and 400 mg/kg body wt respectively. Group VI served as plant control and received extract at a dose of 400 mg/kg body wt. All groups, except groups I and VI, received NaF (100 ppm) through drinking water for 30 days. Results showed that administration of extract significantly minimized elevated serum levels of CK-MB and LDH, decreased cardiac lipid peroxidation, increased levels of reduced glutathione content and catalase enzyme in a dosedependent manner. The study revealed that BOB leaves show moderate antioxidant and alleviated sodium fluoride induced cardiotoxicity.
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