Atherosclerosis is a major contributor to cardiovascular disease, characterized by inflammation and lipid accumulation in arterial walls, leading to plaque formation. Elevated low-density lipoprotein cholesterol is a primary risk factor for atherosclerosis. All-trans retinoic acid (ATRA), a metabolite of vitamin A, has demonstrated anti-inflammatory effects and potential in regulating vascular injury. 9-cisretinoic acid (9cRA) is an active metabolite of vitamin A and activates the retinoid X receptor. This study investigates whether potassium retinoate (PA9RA), a synthetic combination of ATRA and 9cRA, offers superior efficacy in treating atherosclerosis compared to established treatments such as clopidogrel and atorvastatin. Male ApoE -/- mice were fed a Western-type diet and treated with PA9RA, clopidogrel, or atorvastatin for 10 weeks. The body weight, organ weight, serum biochemistry, and histopathology, including atherosclerotic lesion area and liver steatosis were assessed. PA9RA treatment led to a significant reduction in body weight and inguinal fat, with the 45 mg/kg/day dose showing marked efficacy in decreasing atherosclerotic lesion size and ameliorating liver steatosis. Histopathological evaluation revealed decreased foam cell formation and improved liver histology in PA9RA-treated groups compared to controls. Notable side effects included epidermal hyperplasia and gastric hyperplasia at high doses of PA9RA. PA9RA exhibits superior efficacy over clopidogrel and atorvastatin in ameliorating atherosclerosis and fatty liver in ApoE –/–mice. This study highlights PA9RA's potential as a promising therapeutic agent for atherosclerosis. Further research is needed to elucidate its mechanisms of action and assess long-term safety and efficacy.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

Purpose: Smoking may have a protective role in developing ulcerative colitis (UC) but have the opposite effect on Crohn’s disease (CD). This study aimed to determine the risk of developing inflammatory bowel disease (IBD) according to smoking status and onset age of smoking. Materials and Methods: We collected data on the smoking experiences of participants aged 20–39 years who underwent biannual examinations provided by the Korean National Health Screening Program from 2009 to 2012. IBD diagnosis was identified using the National Health Insurance Service. The risk of IBD according to smoking status and onset age of smoking was analyzed after adjusting for major clinical variables. Results: During a median 10.59-year follow-up, the risk of UC in ex-smokers was significantly higher than that in non-smokers, and the earlier ex-smokers started smoking, the higher risk of UC [ex-smokers whose onset age of smoking was <20 years, adjusted hazard ratio (aHR) 1.928, 95% confidence interval (CI)=1.649–2.255; 20–24 years, aHR 1.728, 95% CI=1.541–1.939; 25–29 years, aHR 1.676, 95% CI=1.489–1.887; ≥30 years, aHR 1.226, 95% CI=1.010–1.486]. The risk of UC was significantly lower in current smokers whose onset age of smoking was 25–29 years than in non-smokers (aHR 0.825, 95% CI=0.709–0.959). The risk of CD did not differ according to smoking status and onset age of smoking. Conclusion Ex-smokers who started smoking at a young age have a high risk of UC, even after adjusting for the smoking amount.

Atherosclerosis is a major contributor to cardiovascular disease, characterized by inflammation and lipid accumulation in arterial walls, leading to plaque formation. Elevated low-density lipoprotein cholesterol is a primary risk factor for atherosclerosis. All-trans retinoic acid (ATRA), a metabolite of vitamin A, has demonstrated anti-inflammatory effects and potential in regulating vascular injury. 9-cisretinoic acid (9cRA) is an active metabolite of vitamin A and activates the retinoid X receptor. This study investigates whether potassium retinoate (PA9RA), a synthetic combination of ATRA and 9cRA, offers superior efficacy in treating atherosclerosis compared to established treatments such as clopidogrel and atorvastatin. Male ApoE -/- mice were fed a Western-type diet and treated with PA9RA, clopidogrel, or atorvastatin for 10 weeks. The body weight, organ weight, serum biochemistry, and histopathology, including atherosclerotic lesion area and liver steatosis were assessed. PA9RA treatment led to a significant reduction in body weight and inguinal fat, with the 45 mg/kg/day dose showing marked efficacy in decreasing atherosclerotic lesion size and ameliorating liver steatosis. Histopathological evaluation revealed decreased foam cell formation and improved liver histology in PA9RA-treated groups compared to controls. Notable side effects included epidermal hyperplasia and gastric hyperplasia at high doses of PA9RA. PA9RA exhibits superior efficacy over clopidogrel and atorvastatin in ameliorating atherosclerosis and fatty liver in ApoE –/–mice. This study highlights PA9RA's potential as a promising therapeutic agent for atherosclerosis. Further research is needed to elucidate its mechanisms of action and assess long-term safety and efficacy.

Purpose: Smoking may have a protective role in developing ulcerative colitis (UC) but have the opposite effect on Crohn’s disease (CD). This study aimed to determine the risk of developing inflammatory bowel disease (IBD) according to smoking status and onset age of smoking. Materials and Methods: We collected data on the smoking experiences of participants aged 20–39 years who underwent biannual examinations provided by the Korean National Health Screening Program from 2009 to 2012. IBD diagnosis was identified using the National Health Insurance Service. The risk of IBD according to smoking status and onset age of smoking was analyzed after adjusting for major clinical variables. Results: During a median 10.59-year follow-up, the risk of UC in ex-smokers was significantly higher than that in non-smokers, and the earlier ex-smokers started smoking, the higher risk of UC [ex-smokers whose onset age of smoking was <20 years, adjusted hazard ratio (aHR) 1.928, 95% confidence interval (CI)=1.649–2.255; 20–24 years, aHR 1.728, 95% CI=1.541–1.939; 25–29 years, aHR 1.676, 95% CI=1.489–1.887; ≥30 years, aHR 1.226, 95% CI=1.010–1.486]. The risk of UC was significantly lower in current smokers whose onset age of smoking was 25–29 years than in non-smokers (aHR 0.825, 95% CI=0.709–0.959). The risk of CD did not differ according to smoking status and onset age of smoking. Conclusion Ex-smokers who started smoking at a young age have a high risk of UC, even after adjusting for the smoking amount.

Irritable bowel syndrome (IBS) is a chronic, disabling, and functional bowel disorder that significantly affects social functioning and reduces quality of life and increases social costs. The Korean Society of Neurogastroenterology and Motility published clinical practice guidelines on the management of IBS based on a systematic review of the literature in 2017, and planned to revise these guidelines in light of new evidence on the pathophysiology, diagnosis, and management of IBS. The current revised version of the guidelines is consistent with the previous version and targets adults diagnosed with or suspected of having IBS. These guidelines were developed using a combination of de novo and adaptation methods, with analyses of existing guidelines and discussions within the committee, leading to the identification of key clinical questions. Finally, the guidelines consisted of 22 recommendations, including 3 concerning the definition and risk factors of IBS, 4 regarding diagnostic modalities and strategies, 2 regarding general management, and 13 regarding medical treatment. For each statement, the advantages, disadvantages, and precautions were thoroughly detailed. The modified Delphi method was used to achieve expert consensus to adopt the core recommendations of the guidelines. These guidelines serve as a reference for clinicians (including primary care physicians, general healthcare providers, medical students, residents, and other healthcare professionals) and patients, helping them to make informed decisions regarding IBS management.

Background/Aims: Inflammatory bowel disease (IBD) affects health-related quality of life (HRQoL). The Short Inflammatory Bowel Disease Questionnaire (SIBDQ) score is strongly correlated with HRQoL in IBD patients. This study aimed to assess the factors influencing HRQoL in IBD patients. Methods: In this prospective study, all patients with ulcerative colitis (UC) and Crohn’s disease (CD) completed the SIBDQ at enrollment; some patients also completed a second SIBDQ at follow-up. Multiple linear regression analysis was used to determine associations between SIBDQ scores and clinical factors. Results: A total of 1,020 patients participated (UC, 67%; CD, 33%). The median SIBDQ score was 52 (interquartile range, 44 to 59). In UC patients, the stool frequency (β=–2.333, p<0.001), Physician Global Assessment score (β=–3.950, p<0.001), fecal calprotectin level (β=–4.014, p<0.001), and corticosteroid use (β=–4.809, p=0.006) were negatively correlated with the SIBDQ score. In CD patients, the number of diarrhea episodes per day (β=–1.467, p=0.024) and Crohn's Disease Activity Index score (β=–0.045, p<0.001) were negatively correlated with the SIBDQ score. A total of 202 patients completed the second SIBDQ within a mean of 3.4 years. The distributions of SIBDQ score changes were as follows: decrease >10%, 28%; –10%10%, 43%. In both the initial SIBDQ and follow-up SIBDQ, scores for items pertaining to systemic symptoms (tension and fatigue) were relatively low. Conclusions Bowel movement-related problems significantly affect the HRQoL of both UC and CD patients. IBD patients scored lower on SIBDQ items related to general well-being. After 3 years of follow-up at the IBD clinic, 43% of patients showed a significant improvement in HRQoL.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.

Atherosclerosis is a major contributor to cardiovascular disease, characterized by inflammation and lipid accumulation in arterial walls, leading to plaque formation. Elevated low-density lipoprotein cholesterol is a primary risk factor for atherosclerosis. All-trans retinoic acid (ATRA), a metabolite of vitamin A, has demonstrated anti-inflammatory effects and potential in regulating vascular injury. 9-cisretinoic acid (9cRA) is an active metabolite of vitamin A and activates the retinoid X receptor. This study investigates whether potassium retinoate (PA9RA), a synthetic combination of ATRA and 9cRA, offers superior efficacy in treating atherosclerosis compared to established treatments such as clopidogrel and atorvastatin. Male ApoE -/- mice were fed a Western-type diet and treated with PA9RA, clopidogrel, or atorvastatin for 10 weeks. The body weight, organ weight, serum biochemistry, and histopathology, including atherosclerotic lesion area and liver steatosis were assessed. PA9RA treatment led to a significant reduction in body weight and inguinal fat, with the 45 mg/kg/day dose showing marked efficacy in decreasing atherosclerotic lesion size and ameliorating liver steatosis. Histopathological evaluation revealed decreased foam cell formation and improved liver histology in PA9RA-treated groups compared to controls. Notable side effects included epidermal hyperplasia and gastric hyperplasia at high doses of PA9RA. PA9RA exhibits superior efficacy over clopidogrel and atorvastatin in ameliorating atherosclerosis and fatty liver in ApoE –/–mice. This study highlights PA9RA's potential as a promising therapeutic agent for atherosclerosis. Further research is needed to elucidate its mechanisms of action and assess long-term safety and efficacy.

BACKGROUND/OBJECTIVES: Inflammatory responses are key pathological factors in various canine diseases, making the control of inflammatory responses vital for canine health.This study examined the anti-inflammatory effects of rutin on DH82 cells, a type of canine macrophage, against lipopolysaccharide (LPS)-induced inflammatory responses.MATERIALS/METHODS: The inflammatory in vitro experimental model was established by stimulating canine macrophage DH82 cells with LPS. To evaluate the inflammationpreventative effects of rutin, analyses were conducted using enzyme-linked immunosorbent assay, western blot, and real-time quantitative reverse transcription polymerase chain reaction. RESULTS: Rutin inhibited the LPS-induced increase in the protein and gene levels of proinflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α), while antiinflammatory cytokines (IL-10, transforming growth factor-β1) levels remained unchanged.Furthermore, rutin suppressed the LPS-induced activation of phosphorylated extracellular signal-regulated kinase, Jun N-terminal kinase, inhibitor of nuclear factor kappa B, and nuclear factor kappa B (NF-κB) in DH82 cells. CONCLUSION Rutin exerts anti-inflammatory effects by inhibiting the mitogen-activated protein kinase-NF-κB signaling pathway and reducing the production of pro-inflammatory cytokines in DH82 cells.