Acetic Acid Group Research Articles

Protective effect of evodiamine on acetic acid-induced gastric ulcers in rats through regulation of ROS/ICAM1/Nrf2 signaling pathway

Purpose: To study the effect of evodiamine on the signaling pathway of ROS/ICAM-1/Nrf2 in rats with acetic acid-induced stomach ulcers. Methods: The rats were randomly assigned to five groups containing 10 rats each. Prior to acetic acidinduction of gastric ulcers, omeprazole (4.0 mg/kg/day), low-dose evodiamine (L-EVD, 20 mg/kg/day), and high-dose evodiamine (H-EVD, 40 mg/kg/day) were orally administered to the respective groups for 15 days. Following ulcer induction, the same treatments continued for an additional 7 days, for a total treatment duration of 22 days. The control (0.9 % saline) and acetic acid (model) groups were administered 0.9 % sodium chloride solution (10 mL/kg) for the same period. Thereafter, oxidative stress, inflammatory markers, macroscopic and microscopic evaluations were conducted on the gastric mucosa. Results: The acetic acid group showed significantly higher levels of oxidative and inflammatory markers, as well as damage and degeneration of the gastric mucosa when compared to control group (p < 0.05). However, both low-dose and high-dose evodiamine treatment groups demonstrated significant gastric healing. Administration of low-dose and high-dose evodiamine resulted in significantly lower levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), myeloperoxidase (MPO) and intracellular adhesion molecule-1 (ICAM-1, p < 0.05). Furthermore, evodiamine treatment led to significantly increased levels of glutathione (GSH) and nuclear facterythroid factor 2 (Nrf2). Conclusion: Evodiamine reduces oxidative stress, suppresses inflammatory reactions, and exerts an anti-ulcer effect on acetic acid-induced gastric ulcers in rats by modulating ROS/ ICAM-1/Nrf2 signaling pathway. More studies into the integration of evodiamine into conventional pharmaceutical treatments for gastric ulcers should be conducted.

Opuntia ficus-indica cladodes extract inhibits human neutrophil pro-inflammatory functions and protects rats from acetic acid-induced ulcerative colitis.

The increased production of reactive oxygen species (ROS) by human neutrophils can lead to oxidative imbalances and several diseases, such as inflammatory bowel disease (IBD). Opuntia ficus-indica (O. ficus-indica) is rich in bioactive substances with anti-inflammatory properties. This study aimed to identify the bioactive compounds present in aqueous cladodes extract (ACE) of O. ficus-indica using high-performance liquid chromatography (HPLC) and to test its effects on human neutrophil inflammatory functions and on ulcerative colitis (UC) induced by acetic acid (Aa) in rats. ROS production and degranulation by neutrophils were assessed by luminol-amplified chemiluminescence, enzymatic techniques, and western blotting. In vivo, the experiment involved seven groups of rats: a negative control group (NaCl), the acetic acid group (Aa), and groups treated with oral sulfasalazine (150mg/kg) or various doses of ACE for 7days. Colonic lesions were induced by an intra-rectal Aa injection, and inflammation was assessed. HPLC analysis identified gallic acid, catechin, caffeic acid, and ferulic acid as major compounds in ACE. In vitro, ACE inhibited neutrophil ROS production, including superoxide anion produced by NADPH oxidase, and significantly reduced myeloperoxidase activity and neutrophil degranulation. In vivo, ACE protected rats from Aa-induced histopathological damage of the colonic mucosa, significantly increased catalase, superoxide dismutase and reduced glutathione levels, and significantly suppressed the increases of plasma cytokines (TNF-α and IL-1β) observed in the Aa group. In conclusion, O. ficus-indica ACE has significant anti-inflammatory properties by restoring oxidative balance, indicating that it could be a potential source of therapeutic agents for inflammatory diseases, particularly UC.

Behind the Scenes: Metagenomic Analysis of Bacterial Communities in Sustainable Depilation of Sheepskin.

The leather industry is embracing eco-friendly technologies for both regulatory compliance and sustainable growth. While enzymatic depilation provides a greener alternative to traditional beamhouse methods, its complexity often leads to higher costs. To address this, we examined the performance of sheepskins' native bacterial flora in acetic acid conditions with low environmental impact. Utilizing metagenomic techniques, we analyzed the bacterial community dynamics during the depilation process. This investigation revealed a notable increase in microbial diversity and richness in acetic acid treatments compared to water treatments. At the class level, a post-processing decrease in Gammaproteobacteria dominance was observed, while Actinomycetia numbers surged in the acetic acid group. In contrast, the water group showed an increase in Bacteroidia. Order-level analysis indicated reductions in Pseudomonadales and increases in Actinomycetales with acetic acid treatment, whereas Flavobacteriales was more prevalent in water-treated liquors. At the family level, Moraxellaceae decreased and Micrococcaceae increased in the acetic acid group, in contrast to the marked rise of Weeksellaceae in the water group. Temporal analyses further highlighted the evolving bacterial landscapes under different treatments. Moreover, acetic acid treatment fostered a stable microbial community, beneficial for sustainable leather processing. Functional pathways were predicted using PICRUSt2. It showed that significantly enriched degradation pathways in the water group were less abundant in the acetic acid group, potentially preventing substrate matrix damage during depilation. The study underscores the transformative potential of acetic acid for the leather industry, offering a pathway to reduce pollution while maintaining economic viability. By enhancing our understanding of microbial interactions during depilation, this study opens avenues for refining these eco-friendly techniques. Our findings advocate for a shift towards greener depilation methods and contribute to the broader dialogue on sustainable manufacturing practices, emphasizing the importance of leveraging indigenous microbial communities for environmental and economic gains.

Evaluation of Salvia officinalis in the Treatment of Acetic Acid-Induced Ulcerative Colitis in a Rat Model

Abstract Introduction Ulcerative colitis (UC) is an inflammatory bowel disease that causes long-lasting inflammation and ulcers within the digestive tract. This study aims to determine the histochemical alteration of Salvia officinalis (sage), an anti-inflammatory and antioxidant herbal agent on UC. Materials and Methods The disease was induced in 37 Sprague-Dawley rats with 2 mL of 3% acetic-acid (AA) enema. The rats were divided into five groups: a control group (AA), two 5-aminosalicylic (5-ASA) groups treated either orally (AO) or rectally (AR) with a dose of 100 mg/kg, and two salvia groups treated with 300mg/kg salvia orally (SO) or rectally (SR). Histopathological analyses of the colon were done on day 7, and markers such as C-reactive protein (CRP), superoxide dismutase (SOD), and complete blood count were measured. Result In macroscopic evaluation, the AO group demonstrated the lowest involvement, followed by the SO, SR, AR, and AA groups, respectively (p = 0.01). There was no significant difference between the SO and AO groups (p = 0.10), and the SR and AR groups (p = 0.58). Regarding microscopic histopathological findings, the AO and SO group demonstrated the most satisfactory results, with no significant difference between the AO versus SO, and AR versus SR groups. Inflammation was resolved in all of the AO and SO subjects. Conclusion Salvia can be beneficial in the treatment course of UC by inhibiting inflammatory responses, increasing the growth and viability of intestinal mucosa, and its antioxidant effects. Therefore, we propose the prescription of salvia as an adds-on or alternative therapy in the management of UC.

Divergent histopathological and molecular patterns in chemically induced interstitial cystitis/bladder pain syndrome rat models

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a complex chronic pain disorder with an elusive etiology and nonspecific symptoms. Although numerous animal models with phenotypes similar to human disease have been established, no available regimen can consistently alleviate clinical symptoms. This dilemma led us to question whether current animal models adequately represent IC/BPS. We compared four commonly used IC/BPS rat models to determine their diverse histopathological and molecular patterns. Female rats were given single treatments with hydrochloric acid (HCL), acetic acid (AA), protamine sulfate plus lipopolysaccharide (PS + LPS), or cyclophosphamide (CYP) to induce IC/BPS. Bladder sections were stained for histopathologic evaluation, and mRNA expression profiles were examined using next-generation sequencing and gene set analyses. Mast cell counts were significantly higher in the HCL and AA groups than in the PS + LPS, CYP, and control groups, but only the AA group showed significant collagen accumulation. The models differed substantially in terms of their gene ontology and Kyoto encyclopedia of genes and genomes pathways. Our observations suggest that none of these rat models fully reflects the complexity of IC/BPS. We recommend that future studies apply and compare multiple models simultaneously to fully replicate the complicated features of IC/BPS.

Rutin mitigates acetic acid-induced ulcerative colitis: novel coloprotective mechanism.

Ulcerative colitis, an inflammatory bowel disease, is characterized by a status of oxidative stress and inflammation. Rutin is a natural flavonoid with many pharmacological activities and its role in acetic acid-induced ulcerative colitis through the high mobility group B1 (HMGB1)/ toll-like receptor-4 (TLR4)/ myeloid differentiation primary response protein 88 (MYD88)/ nuclear factor-kB (NF-kB) signaling pathway needs to be explored. Four experimental groups were divided into control group, rutin group: treated with 100mg/kg/day rutin orally for 10days, acetic acid (AA) group: given intracolonic instillation of AA to induce ulcerative colitis, and acetic acid with rutin treatment (AA/Rutin) group. Acetic acid caused a marked increase in the colon weight/length ratio and induced colonic histopathological changes, leading to a marked rise in the colonic histopathological scores. Acetic acid exhibited a significant rise in LDH and CRP serum levels as well as TOS colonic levels, accompanied by a marked decline in TAS colonic contents compared to the control group. Moreover, AA-induced activation of the HMGB1/TLR4/MYD88/NF-kB signaling pathway. Rutin demonstrated a significant decrease in the colon weight/length ratio, ameliorated the colonic histopathological changes induced by AA, and exhibited a marked decline in the colonic histopathological scores. Rutin showed a significant decrease in serum LDH, and CRP levels as well as colonic TOS contents when compared with the AA group. Rutin suppressed the colonic activation of the HMGB1/TLR4/MYD88/NF-kB signaling pathway. Rutin could be a promising coloprotective agent against AA-induced ulcerative colitis by targeting the HMGB1/TLR4/MYD88/NF-kB signaling pathway.

Effect of various surface treatment methods on shear bond strength between acrylic denture teeth and thermoplastic nylon denture base

AbstractPurposeTo evaluate the effect of mechanical, chemical, and mechanical‐chemical surface treatment methods on shear bond strength between acrylic denture teeth and thermoplastic nylon denture base.Materials and MethodsMaxillary central incisor teeth were treated with five different surface treatment methods: mechanical (sandblasting, T‐shape diatoric holes), chemical (5% acetic acid solution, bonding agent), and mechanical‐chemical (sandblasting + bonding agent) were embedded in thermoplastic nylon denture base (n = 10). A universal testing machine with a crosshead speed of 0.5 mm per minute was used to test the shear bond strength. Data obtained were statistically evaluated using one‐way ANOVA and followed with Tukey post hoc test (α = 0.05)ResultsT‐shaped diatoric holes exhibited significantly higher shear bond strength among the surface treatment groups, followed by sandblasting + bonding agent, sandblasting, bonding agent, and the acetic acid group (p < 0.001)ConclusionT‐shaped diatoric holes as a mechanical surface treatment showed higher shear bond strength than other methods.

Comprehensive review on performance, reliability, and roadmap of c‐Si PV modules in desert climates: A proposal for improved testing standard

AbstractDesert regions have emerged as ideal places for GW utility‐scale photovoltaic (PV) module installations because of their ultra‐large spaces, abundance of high‐irradiance sunshine hours, and clear sky. However, the harsh desert climate presents challenges to the reliability and bankability of PV modules. This review provides an in‐depth understanding of the unique desert parameters impact, desert‐induced degradation modes, status, and required properties of the bill of materials (BOMs) and suggestions for the development of desert standards. The review reveals that the climatic conditions in the desert are considerably harsher than those in the moderate climate. The main degradation mechanisms caused by the desert are ultraviolet (UV)‐induced discoloration, thermomechanical flaws of interconnects, and glass abrasion (because of soiling). The development of desert modules may necessitate the use of new‐generation modules with low‐temperature coefficients, high efficiency, high bifaciality, stability under UV light, and elevated temperatures. For the desert module application, options include advanced back sheets and encapsulants that are thermally and UV stable, free of acetic acid groups, and have a low water vapor transfer rate. The degradation modes induced by desert climate are not sufficiently addressed by the present environmental and safety standards through accelerated aging tests. As a result, this article provides a summary of current standards and recommends creating a new testing proposal called the “Hot Desert Test Cycle (HDTC)” sequence that is specific to the desert climate. This comprehensive review catalyzes the PV community to explore novel designs and develop desert PV modules while adhering to localized standards.

Defective UiO-66-NH2 (Zr) for Simultaneous Adsorption of Phosphate and Pb2+ for Hydrogen Peroxide Purification.

Removal of hetero ions from the hydrogen peroxide solution is a crucial step in purifying electronic-grade H2O2. Conventional adsorption materials are challenged to meet the need for the simultaneous adsorption of both anions and cations in solvents. UiO-66 (Zr) modified by acetic acid and amino group for simultaneous adsorption of phosphate and Pb2+ in H2O2 purification was fabricated in this work. The as-prepared defective UiO-66-NH2 (Zr) demonstrated a significant increase in specific surface area and porosity, along with more exposed sites for phosphate and Pb2+ adsorption. The adsorption capacity of De-UiO-66-NH2 for phosphate and Pb2+ in H2O2 solution was 52.28 mg g-1 and 35.4 mg g-1, which is 1.19 times and 1.88 times that of unmodified UiO-66 (Zr), respectively. The trace simultaneous adsorption with both 100 ppb phosphate and Pb2+ showed removal rates of 94.0% and 88.7%, respectively, confirming the practicality of MOF materials in the purification of electronic chemicals. This work highlights the potential of Zr-based MOFs as anionic and cationic simultaneous adsorbents for highly efficient purification of electronic-grade solvents.

Effects of Mannyeon-hwan on Acetic Acid-induced Colitis in Rats

Objectives: This study is designed to verify the effects of Mannyeon-hwan (MNH) on acetic acid-induced colitis in rats.Methods: Colitis was induced in male Sprague-Dawley rats weighing approximately 250 g by injecting acetic acid through the anus. The rats were classified into four groups: normal group, acetic acid (AA) group, AA+MNH (L) (low concentration) group, and AA+MNH (H) (high concentration) group. The body weight, visual evaluation of the colonic mucosa, anatomical histological changes, and changes in the expression of cytokines in the colon tissue were compared and analyzed.Results: Compared with the normal group, weight loss was observed in mice induced with colitis. Compared with the AA group, weight loss recovery occurred in the AA+MNH (L) and AA+MNH (H) groups, and significant changes were observed after the sixth day. In the visual evaluation of the colonic mucosa, a significant decrease in damage indicators was observed in the AA+MNH (L) and AA+MNH (H) groups compared with the AA group. In terms of anatomical histological changes and changes in the expression of tumor necrosis factor-α and interleukin-6 in colon tissue, a significant decrease was observed in the AA+MNH (L) and AA+MNH (H) groups compared with the AA group. A more pronounced decrease was observed in the AA+MNH (H) group compared with the AA+MNH (L) group.Conclusion: The effects of MNH on colitis were confirmed through research. MNH can be used as a first-line treatment for patients complaining of colitis who visit oriental medicine clinics.

Ameliorative effects of androstenediol against acetic acid-induced colitis in male wistar rats via inhibiting TLR4-mediated PI3K/Akt and NF-κB pathways through estrogen receptor β activation

5-androstenediol (ADIOL) functions as a selective estrogen receptor β (ERβ) ligand with a protective effect against many diseases. So, we conducted a novel insight into its role in acetic acid (AA)-induced colitis and investigated its effect on TLR4-Mediated PI3K/Akt and NF-κB Pathways and the potential role of ERβ as contributing mechanisms. Methods: Rats were randomized into 5 Groups; Control, Colitis, Colitis + mesalazine (MLZ), Colitis + ADIOL, and Colitis + ADIOL + PHTPP (ER-β antagonist). The colitis was induced through a rectal enema of acetic acid (AA) on the 8th day. At the end of treatment, colons were collected for macroscopic assessment. Tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), nuclear factor kappa b (NF-κB), toll-like receptor (TLR4), and phosphorylated Protein kinase B (pAKT) were measured. Besides, Gene expression of interleukin-1beta (IL-1β), metalloproteases 9 (Mmp9), inositol 3 phosphate kinase (PI3K), Neutrophil gelatinase-associated lipocalin (NGAL), ERβ and NLRP6 were assessed. Histopathological and immunohistochemical studies were also investigated. Results: Compared to the untreated AA group, the disease activity index (DAI) and macroscopic assessment indicators significantly decreased with ADIOL injections. Indeed, ADIOL significantly decreased colonic tissue levels of MDA, TLR4, pAKT, and NF-κB immunostainig while increased SOD activity and β catenin immunostainig. ADIOL mitigated the high genetic expressions of IL1β, NGAL, MMP9, and PI3K while increased ERβ and NLRP6 gene expression. Also, the pathological changes detected in AA groups were markedly ameliorated with ADIOL. The specific ERβ antagonist, PHTPP, largely diminished these protective effects of ADIOL. Conclusion: ADIOL could be beneficial against AA-induced colitis mostly through activating ERβ.

Gilaburu (Viburnum opulus L.) fruit extract has potential therapeutic and prophylactic role in a rat model of acetic acid-induced oxidant colonic damage

Ethnopharmacological relevanceUlcerative colitis (UC) which has a global impact on the health care system with its recurrent and incompletely curable characteristics, affects the patients’ quality of life. Gilaburu (GB; Viburnum opulus L.) is a fruit with rich polyphenol ingredient which is used ethnobotanically in Türkiye for medicinal purposes (for example, to pass kidney stones, to treat stomach, heart, and liver diseases, hemorrhages, hypertension, ulcers, common cold, tuberculosis, rheumatic and menstrual pain, and diabetes). On the other hand, the effects of GB in the experimental UC model have not been studied. Aim of the studyThis study aimed to explore the potential antioxidant and anti-inflammatory effects of GB fruit extract in improving acetic acid (AA)-induced UC. Materials and methodsStarting immediately after (AA + GB group) or 1 week before (GB + AA + GB group) the colitis induced by intrarectal AA (5%; v/v) administration, the rats orally received GB (100 mg/kg) once per day for 3 days. The control and AA groups were administered orally saline (1 ml), while the AA + SS group were administered sulfasalazine (SS; 100 mg/kg; orally) as a positive control once per day for 3 days. Distal colonic tissue specimens were obtained for the histological and biochemical [myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), chemiluminescence (CL), caspase-3, 8-hydroxy-2’-deoxyguanosine (8-OHdG), matrix metalloproteinase (MMP)-9, transforming growth factor (TGF)-β1, smad-3 and cytokine (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, interferon (IFN)-γ), measurements] evaluations on the 3rd day. ResultsElevated macroscopic and microscopic damage scores, high tissue wet weight values, increased tissue-associated MPO, MDA, CL, caspase-3, 8-OHdG, cytokines (TNF-α, IL-1β, IL-6, IL-8), MMP-9, TGF-β1, smad-3 levels, and decreased GSH values of the AA group were all reversed by GB treatments (AA + GB and GB + AA + GB groups) (p < 0.05–0.001). However, sulfasalazine treatment (AA + SS group) did not change the IL-8, 8-OHdG, MMP-9, and TGF-β1 measurements significantly. ConclusionsGilaburu shows both anti-inflammatory and antioxidant effects against AA-induced colonic damage by suppressing neutrophil infiltration, regulating inflammatory mediators, inhibiting reactive species production, lipid peroxidation, and apoptosis, conserving endogenous antioxidant glutathione, and ameliorating oxidative DNA damage. Since the current ulcerative colitis drugs display limited benefits and adverse side effects, potential therapeutic and/or prophylactic role of gilaburu can be evaluated in ulcerative colitis.

Comparison of the efficacy of 5% versus 8% acetic acid concentrations for detecting premalignant and malignant lesions in colposcopy.

Although preventable; cervical cancer remains a significant cause of morbidity and mortality worldwide, especially in developing countries; thus, early diagnosis and treatment are essential to prevent its development into invasive cancer. Based on the screening results, diagnostic colposcopy was performed to evaluate women with abnormal Papinocalaou test results, high-risk human papillomavirus DNA positivity, or suspected cervical cancer. Therefore, this study aimed to determine the optimal acetic acid concentration (5% or 8%) for detecting cervical precancerous/cancerous lesions during colposcopy evaluation. This study included 607 patients admitted to our obstetrics and gynecology clinic. The medical records of the patients were obtained from the colposcopy registry in the hospital information system and retrospectively analyzed. The cases were divided into 2 groups according to the acetic acid concentrations (5% and 8%) used during colposcopy and examined. The duration of acetic acid application was 2 to 4 minutes. The probability of developing ≥ CIN2 was low in patients with negative for intraepithelial lesion or malignancy smear results in both groups, but increased in the high-grade squamous intraepithelial lesions/atypical squamous cells group with the 8% acetic acid concentration (P < .0001; P = .012). The probabilities of pathological detection of ≥ CIN2 in the 5% and 8% acetic acid groups were 17.3% and 46.6%, respectively (P < .0001). The enhancement of the efficiency of colposcopy should focus on improving the detectability of precancerous lesions. Given that this study compared the effectiveness of acetic acid concentration in colposcopy diagnostics, it can be considered a leading study in this field.

The effect of acetic acid-induced pain in Parkinson’s disease model in zebrafish

Parkinson's disease (PD) is the second most common neurodegenerative disease caused by the degeneration of dopaminergic neurons and the accumulation of Lewy bodies. Pain is one of the most common non-motor symptoms in PD, but the molecular mechanism of pain in PD is not fully understood, which prevents early diagnosis of PD. We aimed to determine the changes in opioidergic pathways when external pain is inflicted by inducing pain intraperitoneally in zebrafish, for which we generated a rotenone-induced PD model. After behavioural analyses in control(C), acetic acid (AA), rotenone (ROT), and rotenone+ acetic acid (ROT+AA) groups, catecholamine levels in brain tissue were determined by LC-MS/MS, expression of opioid peptides and their receptors by RT-PCR, expression of tyrosine hydroxylase by immunohistochemical method, and analyses of oxidant-antioxidant parameters by spectrophotometric methods. In the ROT group, distance travelled, average speed, and brain dopamine levels decreased, while LPO (lipid peroxidation) and NO (nitric oxide) increased as indicators of oxidative damage, and the SOD activity decreased. The mRNA expression of lrrk, pink1, and park7 genes associated with PD increased, while the mRNA expression of park2 decreased. This indicates that rotenone exposure is a suitable means to induce PD in zebrafish. The fact that body curvature was higher in the AA group than in the ROT and ROT+AA groups, as well as the decreased expression of penka, pdyn, and ion channels associated with the perception of peripheral pain in the ROT+AA group, suggest that mechanisms associated with pain are impaired in the rotenone-induced PD model in zebrafish.

Moxifloxacin's Therapeutic Effects in AA-Induced Colitis: Anti-Inflammatory Action through NF-κB Pathway Inhibition, Including TNF-α Pathway and Downstream Inflammatory Processes

Objectives: The aim of the present study was to evaluate possible therapeutic effects of moxifloxacin against acetic acid-induced colitis in a rat model.&#x0D; Methods: Forty adult Wistar rats were separated into 4 groups, including the negative control group, acetic acid (AA) group, AA + sulfasalazine (100 mg/kg/day) group, and AA+ moxifloxacin (MFX) (8 mg/kg/day) group. Experimental colitis was induced in rats by rectal administration of (4%v/v) acetic acid. Rats with colitis were received either MFX 8mg/kg/day or sulfasalazine 100mg/kg orally for 7days.The parameters measured are macroscopical assessment, colon weight (indicator of edema) and the measurement of concentrations of the proinflammatory cytokine TNF-α, oxidative stress marker malondialdehyde (MDA), adhesion molecule selectin and the inflammatory mediator NF-κB in colonic tissue homogenate.&#x0D; Results: This study had shown that AA elevate macroscopical scores, colon weight and biochemical homogenate parameters and all measured parameters were significantly reduced by both moxifloxacin and sulfasalazine with nonsignificant difference between them.&#x0D; Conclusions: The study explain that moxifloxacin possesses therapeutic potential in in AA induced colitis and its anti-inflammatory actions may involve inhibition of NF-κB inflammatory pathways including TNF-α pathway with its downstream inflammatory process such as elevation of adhesion molecule synthesis and oxidative species overproduction in the colonic tissues.

Comparative treatment of Sulfasalazine+Ezetimibe combination and Sulfasalazine in a rat model with induced colitis.

Ulcerative colitis is a chronic inflammatory disease with high mortality and morbidity worldwide. It causes inflammation in the lining of the colon, resulting in several symptoms that negatively impact the quality of life. Unfortunately, there is currently no known cure for this condition. Therefore, it is crucial to explore alternative treatment approaches. This research aimed to investigate the anti-inflammatory and antioxidative effects of a combination therapy involving Sulfasalazine+Ezetimibe compared to Sulfasalazine alone in a rat model of ulcerative colitis. Forty adult rats were divided into four groups for this study. The groups consisted of a control group (negative control), an acetic acid group (positive control), an acetic acid+Sulfasalazine (100 mg/kg per day) group, and an acetic acid+Sulfasalazine (50 mg/kg)+Ezetimibe (5 mg/kg) group. Rats were treated for one week, and colitis was induced by administering 2 ml of 4% (v/v) acetic acid inter-rectally. After sacrifice, the colonic tissue homogenate was analyzed for several markers, including proinflammatory cytokines (TNF-α, IL-1β, NF-κB), oxidative stress markers (malondialdehyde, myeloperoxidase), and adhesive molecule markers (E-selectin, ICAM-1). Sulfasalazine and the combination of Sulfasalazine+Ezetimibe significantly reduced the colonic levels of TNF-α, IL-1β, NF-κB, MDA, and E-selectin in the homogenate. However, the combination therapy of Sulfasalazine and Ezetimibe demonstrated a superior effect.

Comparing the Efficacy of Carvedilol and Celecoxib to Prednisolone in Acetic Acid-Induced Ulcerative Colitis in Male Albino Rats

Ulcerative colitis refers to destruction of mucosal layer of distal colon and rectum. Exact mechanism for pathophysiology is still unclear but inflammation and oxidative stress may play a caustic role. Neutrophil and monocyte infiltration results in free radical generation which damages intestinal mucosa. Many treatments as steroids are used to reduce inflammation but cannot cause remission. Carvedilol is a third-generation nonselective β-blocker which possesses anti-oxidant, anti-inflammatory properties and can reduce gastric ulceration. Celecoxib is a selective cyclooxygenase -2 (COX-2) inhibitor which decrease risk of gastrointestinal bleeding. The current study was designed to compare the efficacy of carvedilol and celecoxib to prednisolone in acetic acid-induced ulcerative colitis model. A total of 40 adult male albino rats were randomly divided into five groups: Control group: Rats received 2 ml of saline transrectal. Acetic acid (AA) group: Rats were transrectal injected with 2ml acetic acid. Prednisolone +AA group: Rats were pre-treated with prednisolone in a dose 4mg/kg /day. Carvedilol +AA group: Rats were pre-treated with carvedilol in a dose 30 mg/kg/day. Celecoxib +AA group: Rats were pre-treated with celecoxib in a dose 5mg/kg/day. All drugs were given orally for 7 days. At end of experiment, distal colon was removed, one part of specimen was preserved in 10% formalin for histological examination and other part was homogenized for evaluation of tumor necrosis factor alpha (TNF-α), reduced glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO) and mitogen-activated protein kinase ( p38 MAPK). Data of present study revealed that treatment of rats with carvedilol or celecoxib before induction of colitis significantly reduced levels of TNF-α, MDA, NO and mRNA level of p38 MAPK while both drugs increased GSH level. Protective effects of Carvedilol and celecoxib are due to anti-inflammatory, anti-oxidant effects and ability to decrease synthesis of MAPK which reduce cytokines signaling in epithelial cells of gut mucosa.

Acetic acid-induced pain elicits stress-, and camouflage-related responses in zebrafish: Modulatory effects of opioidergic drugs on neurobehavioral phenotypes

While pain results from the activation of nociceptors following noxious stimuli, mounting evidence links pain- and stress-related responses in mammals. In zebrafish, the activation of hypothalamic-pituitary-interrenal (HPI) axis may also regulate body pigmentation (the camouflage response). Here, we aimed to investigate a putative relationship between pain-, stress-, and camouflage-related parameters in adult zebrafish. To answer this question, we assessed whether intraperitoneal acetic acid injection can activate the HPI axis, measuring whole-body cortisol and the camouflage response as physiological endpoints in the presence or absence of morphine or naloxone, an opioid antagonist. Acetic acid induced a stereotypic circling behavior in the top of the tank, accompanied by abdominal writhing-like response, a specific phenotype that reflects local nociceptive effect. Both whole-body cortisol levels and camouflage response increased in the acetic acid group, while morphine prevented these responses, and naloxone antagonized morphine-induced effects. Moreover, we observed positive correlations between representative behavioral, physiological and skin coloration endpoints, and a “pain index” was proposed to summarize phenotypic profile of zebrafish under different pharmacological manipulations. Collectively, these findings suggest a coordinated activation of pain, camouflage- and stress-related pathways following acetic acid injection in zebrafish. Our data also support that camouflage response represents a novel and relevant biomarker for future probing pain and stress neurobiology, with a robust sensitivity to opioidergic drugs.

A Chemically Induced Experimental Colitis Model with a Simple Combination of Acetic Acid and Trinitrobenzene Sulphonic Acid.

It was aimed to induce a new experimental colitis model by using acetic acid and trinitrobenzene sulphonic acid together and to investigate the severity of inflammation biochemically and histopathologically in comparison with other models. Fifty-six Wistar albino male rats were randomly divided into 4 groups as control, acetic acid, trinitrobenzene sulphonic acid, and combined groups, and the animals were sacrificed following the induction of colitis on the third day and on the seventh day. The serum amyloid A and myeloperoxidase were tested in plasma samples, and the tumor necrosis factor-alpha, interleukin 33, and ST2 were assayed in colon tissue samples with enzyme-linked immunosorbent assay in addition to histopathological examination. There were statistically significant differences between the combined and the control groups both on the third day and on the seventh day in all parameters. There was no difference between the acetic acid group on the seventh day and the control groups in biochemical parameters. The acetic acid model forms acute colitis. The combined model is found to be more successful in forming inflammation when compared to other models.

Behavioral toxicity, histopathological alterations and oxidative stress in Tubifex tubifex exposed to aromatic carboxylic acids- acetic acid and benzoic acid: A comparative time-dependent toxicity assessment

This study evaluated Acetic acid (AA) and Benzoic acid's (BA) acute and sublethal toxicity by observing mortality, behavioral responses, and changes in the levels of oxidative stress enzymes in Tubifex tubifex. Exposure-induced changes in antioxidant activity (Catalase, Superoxide dismutase), oxidative stress (Malondialdehyde concentrations), and histopathological alterations in the tubificid worms were also noted across exposure intervals. The 96 h LC50 values of AA and BA to T. tubifex were 74.99 and 37.15 mg/l, respectively. Severity in behavioral alterations (including increased mucus production, wrinkling, and reduction in clumping) and autotomy showed concentration-dependent trends for both toxicants. Although histopathological effects also showed marked degeneration in the alimentary and integumentary systems in highest exposure groups (worms exposed to 14.99 mg/l for AA and 7.42 mg/l for BA) for both toxicants. Antioxidant enzymes (catalase and superoxide dismutase) also showed a marked increase of up to 8-fold and 10-fold for the highest exposure group of AA and BA respectively. While species sensitivity distribution analysis revealed T. tubifex as most sensitive to AA and BA compared to other freshwater vertebrates and invertebrates, General Unified Threshold model of Survival (GUTS) predicted individual tolerance effects (GUTS-IT), with slower potential for toxicodynamic recovery, as a more likely pathway for population mortality. Study findings demonstrate BA with greater potential for ecological effects compared to AA within 24 h of exposure. Furthermore, ecological risks to critical detritus feeders like T. tubifex may have severe implications for ecosystem services and nutrient availability within freshwater habitats.