• Journal of Ginseng Research
• /
• v.43 no.3
• /
• pp.335-341
• /
• 2019

Background: Inflammation is a host-defensive innate immune response to protect the body from pathogenic agents and danger signals induced by cellular changes. Although inflammation is a host-defense mechanism, chronic inflammation is considered a major risk factor for the development of a variety of inflammatory autoimmune diseases, such as rheumatic diseases. Rheumatic diseases are systemic inflammatory and degenerative diseases that primarily affect connective tissues and are characterized by severe chronic inflammation and degeneration of connective tissues. Ginseng and its bioactive ingredients, genocides, have been demonstrated to have antiinflammatory activity and pharmacological effects on various rheumatic diseases by inhibiting the expression and production of inflammatory mediators. Methods: Literature in this review was searched in a PubMed site of National Center for Biotechnology Information. Results: The studies reporting the preventive and therapeutic effects of ginseng and ginsenosides on the pathogenesis of rheumatic diseases were discussed and summarized. Conclusion: Ginseng and ginsenosides play an ameliorative role on rheumatic diseases, and this review provides new insights into ginseng and ginsenosides as promising agents to prevent and treat rheumatic diseases.

• 월간산업보건
• /
• s.350
• /
• pp.47-59
• /
• 2017

• Journal of Korean Neurosurgical Society
• /
• v.67 no.4
• /
• pp.485-485
• /
• 2024

• Childhood Kidney Diseases
• /
• v.21 no.2
• /
• pp.156-159
• /
• 2017

Systemic lupus erythematosus (SLE) is characterized by various symptoms and multi-organ involvement. Hypophosphatemia has been described in several diseases accompanied with systemic inflammation. However, hypophosphatemia has rarely been described in SLE patients, especially in those without nephritis. We report the case of a 13-year-old girl with SLE who developed hypophosphatemia without renal involvement. Her hypophosphatemia was caused by renal loss of phosphorus and persisted for 7 months. It improved as her complement levels increased. Therefore, hypophosphatemia may be related to disease activity in SLE patients.

• Natural Product Sciences
• /
• v.25 no.3
• /
• pp.215-221
• /
• 2019

Inflammation is the crucial biological process of immune system which acts as body's defense and protective response against the injuries or infection. However, the systemic inflammation devotes the adverse effects such as multiple inflammation associated diseases. One of the best ways to treat this entity is by blocking the tumor necrosis factor alpha ($TNF-{\alpha}$) and TNF-related apoptosis-inducing ligand (TRAIL) to avoid the proinflammation cytokines production. Thus, this study aims to evaluate the potency of Sambucus bioactive compounds as anti-inflammation through in silico approach. In order to assess that, molecular docking was performed to evaluate the interaction properties between the $TNF-{\alpha}$ or TRAIL with the ligands. The 2D structure of ligands were retrieved online via PubChem and the 3D protein modeling was done by using SWISS Model. The prediction results of the study showed that caffeic acid (-6.4 kcal/mol) and homovanillic acid (-6.6 kcal/mol) have the greatest binding affinity against the $TNF-{\alpha}$ and TRAIL respectively. This evidence suggests that caffeic acid and homovanillic acid may potent as anti-inflammatory agent against the inflammation associated diseases. Finally, this study needs further examination and evaluation to validate the potency of Sambucus bioactive compounds.

• Biomolecules & Therapeutics
• /
• v.19 no.4
• /
• pp.466-471
• /
• 2011

Allergic asthma is complex inflammatory airway disorder caused by genetic and environmental factors. Sulfamethoxazole, a sulfonamide, is the cause of drug rash with eosinophilia and systemic symptoms syndrome. Parasites infection also related with eosinophilia and allergic diseases. In the present study, we investigated the modulating effects of parasitic derivative and sulfamethoxazole (SMX) on allergic airway inflammation in the ovalbumin (OVA)-induced murine asthma model. Histopathological changes, cytokine secretion, and total and allergen-specific IgE were investigated. BALB/c mice were treated with Ascaris suum extract or SMX for 4 weeks before sensitized and challenged to ovalbumin. Pre-treatment of Ascaris suum extract decreased allergic inflammation in lung tissue and IL-4, total IgE, and OVA-specific IgE levels in bronchoalveolar lavage fluid. However, pre-treatment of SMX did not show any effects on allergic airway inflammation. These results indicate that parasitic infection has protective effects on allergic asthma, but the sulfamamides may not relate with allergic asthma.

• Maxillofacial Plastic and Reconstructive Surgery
• /
• v.35 no.4
• /
• pp.236-242
• /
• 2013

Purpose: The objective of this retrospective study is to evaluate the factors affecting the spread of odontogenic infection. Furthermore, this study was performed to apply to future treatments. Methods: A total of 65 patients, who had received treatment for odontogenic infections from 2010 to 2012 for 3 years, were enrolled in this study. The causes of infection, presence of systemic disease, and complications, durations of treatment, treatment methods, and inflammation levels were compared with the data. Results: Patients over 70 years with systemic disease required immediate drainage, systemic antibiotic therapy and hospitalization. We can determine the direction of the early diagnosis and treatment through blood tests (white blood cells, neutrophil, C-reactive protein [CRP]) and computed tomography. Patients over 70 years with systemic disease had the highest percentage. In addition, these patients showed high levels of inflammation index, such as CRP average of 24.8 and needed for a long-term treatment period and a wide range of surgical incision & drainage several times. Systemic diseases, particularly diabetes mellitus and hypertension, accelerate the spread of infection and had a negative effect that delays healing. Eventually, five of the 65 patients showed serious systemic complications. Conclusion: When evaluating cervico-facial infected patients due to odontogenic infection, the most important thing is deciding the appropriate diagnosis and degree of disease. Considering the patient's systemic status and age, we need to decide the treatment plan. Especially, those patients over 70 years with systemic disease should be treated with rapid surgical approach, and the use of a wide range of antibiotics and intensive care. If proper treatment principle does not apply, severe life-threatening complications will result, such as necrotizing fascitis, acute airway obstruction, mediastinitis, and others.

• Toxicological Research
• /
• v.31 no.1
• /
• pp.49-59
• /
• 2015

Eye is a highly vascularised organ. There are chances that a foreign substance can enter the systemic circulation through the eye and cause oxidative stress and evoke immune response. Here the eyes of rabbits were exposed, for a period of 7 days, to 5 known ocular irritants: Cetyl pyridinium chloride (CPC), sodium salicylate (SS), imidazole (IMI), acetaminophen (ACT) and nicotinamide (NIC). The eyes were scored according to the draize scoring. Blood collected from the treated rabbit were analyzed for haematological and biochemical parameters. After sacrifice, histological analysis of the eye and analysis of pro-inflammatory biomarkers ($IL-1{\alpha}$, $IL-1{\beta}$, IL-8 and $TNF-{\alpha}$) in the cornea using ELISA was carried out. Spleen was collected and the proliferation capacities of spleenocytes were analyzed. Liver and brain were collected and assessed for oxidative stress. The eye irritation potential of the chemicals was evident from the redness and swelling of the conjunctiva and cornea. Histopathological analysis and ELISA assay showed signs of inflammation in the eye. However, the haematological and biochemical parameters showed no change. Spleenocyte proliferations showed only slight alterations which were not significant. Also oxidative stress in the brain and liver were negligible. In conclusion, chemicals which cause ocular irritation and inflammation did not show any systemic side-effects in the present scenario.

• International Journal of Oral Biology
• /
• v.38 no.3
• /
• pp.87-92
• /
• 2013

Periodontal inflammation increases the risk of tooth loss, particularly in cases where there is an associated loss of alveolar bone and periodontal ligament (PDL). Histological and morphometric evaluation of periodontal inflammation is difficult. Especially, the lengths of the periodontal ligament and interdental alveolar bone space have not been quantified. A quantitative imaging procedure applicable to an animal model would be an important clinical study. The purpose of this study was to quantify the loss of alveolar bone and periodontal ligament by evaluation with micro-computed tomography (micro-CT). Another purpose was to investigate differences in infections with systemic E. coli LPS and TNF-${\alpha}$ on E. coli lipopolysaccharide (LPS) in loss of alveolar bone and periodontal ligament model on mice. This study showed that linear measurements of alveolar bone loss were represented with an increasing trend of the periodontal ligament length and interdental alveolar process space. The effects of systemic E. coli LPS and TNF-${\alpha}$ on an E. coli LPS-induced periodontitis mice model were investigated in this research. Loss of periodontal ligament and alveolar bone were evaluated by micro-computed tomography (micro-CT) and calculated by the two- and three dimensional microstructure morphometric parameters. Also, there was a significantly increasing trend of the interdental alveolar process space in E. coli LPS and TNF-${\alpha}$ on E. coli LPS compared to PBS. And E. coli LPS and TNF-${\alpha}$ on E. coli LPS had a slightly increasing trend of the periodontal ligament length. The increasing trend of TNF-${\alpha}$ on the LPS-induced mice model in this experiment supports the previous studies on the contribution of periodontal diseases in the pathogenesis of systemic diseases. Also, our findings offer a unique model for the study of the role of LPS-induced TNF-${\alpha}$ in systemic and chronic local inflammatory processes and inflammatory diseases. In this study, we performed rapidly quantification of the periodontal inflammatory processes and periodontal bone loss using micro-computed tomography (micro-CT) in mice.

• BMB Reports
• /
• v.53 no.1
• /
• pp.10-19
• /
• 2020

Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. The AD pathophysiology entails chronic inflammation involving innate immune cells including microglia, astrocytes, and other peripheral blood cells. Inflammatory mediators such as cytokines and complements are also linked to AD pathogenesis. Despite increasing evidence supporting the association between abnormal inflammation and AD, no well-established inflammatory biomarkers are currently available for AD. Since many reports have shown that abnormal inflammation precedes the outbreak of the disease, non-invasive and readily available peripheral inflammatory biomarkers should be considered as possible biomarkers for early diagnosis of AD. In this minireview, we introduce the peripheral biomarker candidates related to abnormal inflammation in AD and discuss their possible molecular mechanisms. Furthermore, we also summarize the current state of inflammatory biomarker research in clinical practice and molecular diagnostics. We believe this review will provide new insights into biomarker candidates for the early diagnosis of AD with systemic relevance to inflammation during AD pathogenesis.