Abstract: Wernicke’s encephalopathy (WE) is a rare, acute neurological condition that develops due to thiamine deficiency in pregnant women with severe hyperemesis gravidarum (HG). This is a case report of a 28-year-old woman at 17 weeks of gestation with a prior spontaneous abortion and a history of laparotomy surgery to treat infertility. The patient had three out of four diagnostic requirements as put by the European Federation of Neurological Societies. Brain magnetic resonance imaging (MRI) showed symmetrical medial thalamic hyperintensities consistent with WE. Notably, thyroid function tests revealed gestational thyrotoxicosis, which contributed to HG severity but did not explain the cerebellar dysfunction or characteristic MRI changes, indicating superimposed thiamine deficiency and coexistence of HG-related thyrotoxicosis and WE. WE is significantly underdiagnosed in the nonalcoholic population, especially in pregnant women who generally have a high demand for thiamine. This case highlights the need to consider WE in pregnant women presenting with prolonged HG and to initiate parenteral thiamine promptly to prevent irreversible neurological injury.
Abstract: BACKGROUND: Colorectal cancer (CRC) is a malignant tumor that develops in the colon or rectum, usually originating from abnormal growth of cells in the intestinal lining. Pinoresinol diglucoside (PDG) is a lignan compound, which exhibits various pharmacological activities, such as anti-inflammatory, antioxidant, antihypertensive, and anticancer. The aim of the current study was to explore the anticancer effect of PDG against 1,2-dimethylhydrazine (DMH)-induced CRC. MATERIALS AND METHODS: Subcutaneous administration of DMH (20 mg/kg) was used for the induction of CRC in the rats, and the rats were received the oral administration of PDG (2.5, 5, and 10 mg/kg) for 15 weeks. The body weight, colon weight, colon length, cancer marker, phase I, II, antioxidant, cytokines, and inflammatory parameters were estimated. The messenger ribonucleic acid expression and histopathology study were also performed. The gut microbiota was estimated in the facal of all group rats. RESULTS: PDG treatment significantly ( P < 0.001) improved the body weight, colon length, and colon weight, along with a reduction in the level of cancer markers such as tissue polypeptide-specific antigen, tumor-associated glycoprotein 72, carcinoembryonic antigen, and carbohydrate antigen 19.9. PDG treatment also altered the level of alkaline phosphatase, lactate dehydrogenase, phase I and II enzymes, antioxidant parameters, cytokines, and inflammatory parameters, respectively. PDG treatment significantly ( P < 0.001) altered the F/B ratio and relative abundance of Bacteroidetes, Firmicutes , Actinobacteriota, and Desulfobacterota and altered the histopathological alteration. CONCLUSION: PDG exhibited a chemoprotective effect against DMH-induced CRC via regulation of the nuclear factor-kappa B/inducible nitric oxide synthase/cyclooxygenase-2 signaling and gut dysbiosis.
Abstract: BACKGROUND: Diabetes-induced abnormal wound healing is characterized by prolonged oxidative stress, inflammation, and impaired tissue regeneration, largely due to excessive production of oxidative stress and inflammatory mediators. Glyburide is a well-known antidiabetic drug. In this experimental study, we scrutinized the protective effect of glyburide against streptozotocin (STZ) induced wound healing in rats and explored the underlying mechanism. MATERIALS AND METHODS: Swiss Wistar rats were randomly assigned to groups and intraperitoneally injected with STZ to induce diabetes. The rats received the oral administration of glyburide (1.25, 2.5, and 5 mg/kg). We estimated the wound area, body weight, glucose level, insulin level, food intake, water intake, protein, albumin, glucosamine, hydroxyproline, collagen, macrophage migration inhibitory factor (MIF), hexosamine, lipid parameters, antioxidant parameters, apoptosis parameters, inflammatory cytokines, and inflammatory parameters. The mRNA expression levels were estimated in the rats’ skin. RESULTS: Dose-dependent treatment of glyburide decreased the wound area, glucose level, food intake, and water intake, and enhanced the body weight and insulin. Glyburide treatment altered the level of protein, albumin, glucosamine, hydroxyproline, collagen, MIF, hexosamine, lipid parameters (total cholesterol, triglyceride, low-density lipoprotein (LDL), and high-density lipoprotein, very LDL), oxidative stress (malonaldehyde, glutathione, glutathione peroxidase, superoxide dismutase, and catalase), inflammatory cytokines (tumor necrosis factor-α, interleukin-1 β (IL-1 β), IL-6, IL-10, and IL-17), apoptosis parameters (B-cell lymphoma 2 [Bcl-2]-associated X protein [Bax], Bcl-2, cysteine-aspartic acid protease 3 [caspase-3]), inflammatory parameters (cyclooxygenase-2, prostaglandin (PGE 2 ), inducible nitric oxide synthase, nuclear kappa B factor (NF-κB), transforming growth factor-β [TGF-β]). Glyburide treatment altered the mRNA expression of cellular jun (c-Jun), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), chemokine-1 (CXCL1), chemokine-2 (CXCL2), tyrosine kinase with immunoglobulin-like and EGF-like domains Tyrosine Kinase (Tie-2), angiopoietin-1, mothers against decapentaplegic homolog 2 and 3 (Smad2/3), and Transforming growth factor-beta (TGF-β). CONCLUSION: The result clearly showed the protective effect of glyburide against STZ-induced diabetic wound via alteration of NF-κB/TGF-β and c-Jun/PDGF-VEGF Signaling Pathways.
Abstract: BACKGROUND: Inflammatory bowel disease (IBD) is a chronic, progressive, and disabling disorder that includes ulcerative colitis and Crohn’s disease, characterized by periods of remission and relapse. Pharmacological management is the primary treatment option with the goal to induce mucosal healing and reduce relapse rates. OBJECTIVES: The main objective of the present study was to determine the pattern of pharmacotherapy and to evaluate the factors that predict clinical remission in patients with IBD. MATERIALS AND METHODS: A cross-sectional analysis was conducted involving fifty participants diagnosed with IBD. All the participants met predefined study inclusion criteria and voluntarily provided written informed consent. Data encompassing patient demographics, clinical parameters, prescribed medications, and ADRs were collected. The disease activity was evaluated using Simple Clinical Colitis Activity Index/Harvey-Bradshaw Index score. Univariate and multivariate logistic regression analysis was done to assess predictors of clinical remission. RESULTS: The commonly prescribed drugs were mesalamine in 72%, steroids in 50%, and azathioprine in 46% patients. 30% patients had an ADR to the prescribed drug; the most common ADR was anemia and pancytopenia with azathioprine use. 52% patients were in clinical remission. Univariate analysis identified medication adherence as a significant predictor, which was confirmed on multivariate analysis. Patient’s adherent to medication were 32 times more likely to be in remission compared to nonadherent patients. CONCLUSION: Mesalamine and azathioprine were the most commonly prescribed monotherapy drugs. The most frequently prescribed combination therapies were mesalamine in conjunction with either steroids or azathioprine. Adherence to medication was the only factor statistically significantly linked to achieving clinical remission of the disease.
Abstract: BACKGROUND: Glucocorticoids (GCs) are used in the treatment of asthma, autoimmune and allergic disease, but long-term GC therapy increased the bone resorption, oxidative stress, inflammation, and impaired bone formation. Aromadendrin is a flavonol (flavonoid) exhibited the potent effect against oxidative stress and inflammatory disease. The aim of the experimental study was to investigate the antiosteoporosis effect of aromadendrin against dexamethasone (DEX) induced osteoporosis (OS) in the rats. MATERIALS AND METHODS: Female Sprague Dawley rats were used in this study and subcutaneous administration of DEX (2.5 mg/kg/day) was used for the induction of OS in the rats. The rats were received the oral administration of aromadendrin (2.5, 5 and 10 mg/kg) and alendronate for 20 weeks. The body weight, organ weight, transverse diameter, bone length, microcomputed tomography (MicroCT) parameters, oxidative stress parameters, inflammatory cytokines, caspase parameters, inflammatory parameters and messenger ribonucleic acid (mRNA) expression were estimated. RESULTS: Aromadendrin treatment improved the body weight and altered the organ weight (vagina, uterus, and femoral weight); bone weight, transverse diameter, bine length, bone mineral density and bone mineral content level. Aromadendrin altered the level of MicroCT parameters, bone parameters (osteocalcin [OC], border gateway protocol, tartrate-resistant acid phosphatase, beta-CrossLaps, alkaline phosphatase, acid phosphatase); nutrient (phosphorus, magnesium, calcium, 1,25(OH)2-vitamin D 3 ); hormone level (calcitonin, parathyroid hormone, E 2 ), oxidative stress, inflammatory cytokines, inflammatory parameters (nuclear factor-κB [NF-κB], C-reactive protein, monocyte chemoattractant protein-1); caspase parameters (caspase-3, caspase-8, caspase-9), receptor activator of nuclear factor B ligand (RANKL), Osteoprotegerin (OPG), and OPG/RANKL ratio, respectively. Aromadendrin treatment altered the mRNA expression of RANKL, OPG, OPG/RANKL ratio. CONCLUSION: Aromadendrin exerts an anti-OS effect against DEX-induced OS in rats via alteration of NF-κB and RANKL/OPG signaling pathway.
