NSAIDs
Explore 6 research publications tagged with this keyword
Publications Tagged with "NSAIDs"
6 publications found
2026
1 publicationPeptic Ulcer Disease: Mechanisms of Pathogenesis and Insights into Herbal versus Synthetic Treatments
Peptic ulcer disease remains a pressing health issue worldwide, most often linked to Helicobacter pylori infection and long-term use of non-steroidal anti-inflammatory drugs (NSAIDs). While conventional therapies such as proton pump inhibitors (PPIs), histamine-2 receptor antagonists (H2RAs), cytoprotective agents, and antibiotics have transformed patient care by reducing acid secretion and eradicating infection, they are not without drawbacks. Rising antibiotic resistance, drug-related side effects, and recurrence of ulcers continue to challenge clinicians and patients alike. In recent years, herbal medicine has gained attention as a complementary or alternative approach. Plant-derived compounds rich in flavonoids, tannins, alkaloids, and terpenoids offer anti-inflammatory, antioxidant, and antisecretory effects, while also strengthening the stomach’s natural defenses. Traditional remedies such as Anogeissus latifolia, Alchornea castaneaefolia, Decalepis salicifolia, Solanum nigrum, Ocimum tenuiflorum, Asparagus racemosus, and Curcuma longa have shown promising results in experimental models, not only reducing ulcer formation but also accelerating healing. This review brings together evidence on both synthetic and herbal strategies, comparing their mechanisms, effectiveness, safety, and cost considerations. While PPIs and antibiotic regimens remain indispensable for H. pylori eradication and NSAID-induced ulcer prevention, herbal therapeutics stand out for their lower side-effect profile and potential to provide long-term mucosal protection. Looking ahead, integrated treatment approaches that combine modern pharmacology with traditional phytomedicine may offer the most balanced and sustainable path for managing peptic ulcer disease.
2018
1 publicationSolubility Enhancement of Aceclofenac by Solid Dispersion
The aim of the study was to improve the solubility of aceclofenac, which is poorly water soluble drug belongs to BCS class-II. Aceclofenac appears to be particularly well tolerated among the NSAIDs, with a lower incidence of gastrointestinal adverse effects. For poorly soluble orally administered drugs, the rate of absorption is often controlled by the rate of dissolution. To improve the solubility of drug by solid dispersions were prepared with different methods like physical mixture, kneading method and solvent evaporation method with various carriers like poloxamer188, poloxamer407 and PEG 6000 in different ratios from 1:1 to 1:5. The prepared formulations were evaluated for physicochemical characteristics, characterized by differential scanning calorimetry (DSC), X-ray diffraction (XRD), in-vitro dissolution studies and saturation solubility. Based on the evaluation parameters poloxamer407 in ratio of 1:5 through solvent evaporation method was optimized and formulated into tablets by direct compression method. These tablets showed a higher in-vitro dissolution drug release which is 99.62% in 30 minutes when compared with pure drug which showed 26.62% in 60 minutes, whereas marketed tablet (Hifenac) shows 99.64±0.10% in 40 minutes. Hence it was concluded that solid dispersion of aceclofenac drug by using polaxamer 407 with solvent evaporation method enhances solubility, absorption rate and increase bioavailability of the aceclofenac drug.
2015
1 publicationEfficacy of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), Muscle Relaxants and Neurotropic Drugs in Patients with Low Back Pain
To assess efficacy of different classes of drugs in therapy of low back pain. A prospective observational study was carried out over a period of 12 months in which a total of 300 patients with low back pain were enrolled and divided equally into three groups – group 1 (NSAIDs), group 2 (muscle relaxant ±NSAIDs) and group 3 (muscle relaxant ± NSAIDs ± neurotropic drugs). Efficacy of drugs was assessed using oswestry low back disability questionnaire at baseline, 3 weeks and 6 weeks, and the disability index was calculated. There was a male predominance in the study population with a mean age of 39.76 ± 9.40 years. Mean percentage reduction in disability index was maximum in group 2 (54.66±9.85), followed by group 3 (51.33 ± 6.95) and group 1 (46.78 ± 10.12). A significant inter-group difference (p
2014
1 publicationCyclooxygenase-Independent Mechanism of Nonsteroidal Anti-Inflammatory Drugs
A potential mechanism of NSAID-mediated anti-proliferative activity may be through the induction of NAG-1. The present study was conducted to investigate the possible role of selective and non-selective COX inhibitors in inflammation associated angiogenesis and apoptosis. Wistar rats were classified into 5 experimental groups; 9 rats each. Group (1) normal control and group (2) injected s.c. with 0.3 % carrageenan in muscle. Groups (3, 4 and 5) were injected s.c. with carrageenan and at the same time given orally 10 mg/Kg Celecoxib, 12.5 mg/Kg Nimesulide or 10 mg/Kg Sulindac, respectively. NAG-1 gene expression in the liver was measured by RT-PCR. Serum TNFα and muscle caspase-3 were measured by ELISA.Immunohistochemical detection of VEGF in the muscle was investigated. Carrageenan untreated rats showed insignificant change in NAG-1 gene expression compared with control group. Serum TNFα and muscle caspase-3 as well as VEGF expression in carrageenan untreated group were significantly increased compared with normal control rats. In Sulindac treated group, NAG-1 gene expression in the liver and muscle caspase-3 were significantly increased compared with Celecoxib and Nimesulide groups. TNFα serum level was significantly decreased in Nimesulide and Celecoxib treated groups compared with carrageenan and Sulindac groups. The examined NSAIDs proved proapoptotic and antiangiogenic effects.
2013
1 publicationDevelopment of Cross-Linked Alginate Beads by Ionotropic Gelation Technique for Controlled Release of Diclofenac Sodium
The aim of the study was to formulate colon targeted diclofenac sodium alginate beads. The beads were formulated by ionotropic gelation using sodium alginate as polymer, calcium carbonate as an internal cross linking agent and calcium chloride as an external cross linking agent. The optimized beads contained Neusilin and coated with Eudragit L100. The beads were analyzed in terms of, encapsulation efficiency (EE%), particle size and morphology. Swelling properties were studied in simulated gastric fluid (SGF, pH 1.2) and simulated intestinal fluid (SIF, pH 7.4). In vitro drug release was studied in SGF, pH 1.2, SIF, pH 6.8 and SIF, pH 7.4. The results show that the particle size of the beads ranged from 1.98 ± 0.40 to 2.80 ± 0.30 mm. The optimized batch containing Neusilin® had the highest EE% of 72 % significantly higher than other batches (p < 0.05). The degree of swelling of the beads was zero in SGF and about 90 % in SIF at 100 min. The results of the in vitro release showed that the beads had 0 % release in SGF, pH, 1.2 at 2 h, about 3 % in SIF, pH 6.8 at 4 h and 9 % drug release in SIF, pH 7.4 at 9 h. Therefore, sodium alginate beads could be used for colon delivery of diclofenac sodium.Â
2012
1 publicationCyclooxygenase-3: A Review
A continued need to develop safe and effective analgesics and anti-inflammatory drugs fuels the ongoing investigations of cyclooxygenase (COX). Since the early 1990s, it has been appreciated that there are two cyclooxygenase enzymes, cyclooxygenase-1 and cyclooxygenase-2, responsible for the production of prostaglandin H2, the first step in prostanoid biosynthesis. Cyclooxygenase-1 was responsible for the physiological production of prostanoids and cyclooxygenase- 2 was responsible for the elevated production of prostanoids that occurred in sites of disease and inflammation COX-3 is an enzyme that is encoded by the PTGS1 (COX1) gene and is the third and most recently discovered cyclooxygenase (COX) isozyme. The COX-3 isozyme is encoded by the same gene as COX-1, with the difference that COX-3 retains an intron that is not retained in COX-1. In dogs the resulting protein resembles the other two COX enzymes, but in mice and humans it does not, owing to a frame-shift mechanism. Key words: Cyclooxygenase, COX-3, Prostaglandins, Inflammation, NSAIDs Â
