• Journal of Life Science
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• v.21 no.9
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• pp.1310-1314
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• 2011

Anti-inflammatory activities of septicine, a natural alkaloid product present in the leaves and stems of Tylophora ovata, were evaluated in lipopolysaccharide (LPS)-stimulated murine macrophages, RAW264.7 cells. Treatment with septicine inhibited LPS-induced nitric oxide (NO), inflammatory cytokines, tumor necrosis factor-${\alpha}$ and interleukin-6 production in a concentration-dependant manner. In addition, septicine suppressed the expression of inducible NO synthase. These results suggest that the anti-inflammatory activities of septicine might be attributed to the inhibition of NO, iNOS and cytokine expression.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.3
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• pp.297-302
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• 1997

Higenamine was widely used as traditional remedy for the treatment of rhumatoid arthritis. Nitric oxide(NO) may be a critical mediator in this inflammatory disease. Synovial tissue from humans with inflammatory arthritis expresses NOS2(iNOS) mRNA and protein, and generates NO in vitro. We therefore, investigated the effect of higenamine on the induction of nitric oxide synthase(NOS) promoted by lipopolysaccharide(LPS). Prophylactic application of higenamine selectively prevented LPS-primed initiation of L-arginine-induced relaxation and restored rhenylephrine(PE)-induced contraction in rat aorta. LPS-stimulated nitrite production in the incubation medium was reduced by higenamine. Furthermore, RT-PCR and Northern analysis indicated that higenamine reduced iNOS expression primed by LPS in rat aorta. These results suggest that higenamine prevents LPS-promoted induction of NOS in vascular smooth muscle.

• Korean Journal of Veterinary Research
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• v.59 no.2
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• pp.75-80
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• 2019

Enrofloxacin, a fluoroquinolone, is a broad-spectrum antibiotic widely used in veterinary medicine that inhibits the action of bacterial DNA gyrase, resulting in anti-bacterial effects. This study was performed to examine whether enrofloxacin has modulatory and anti-inflammatory activity on immune cells. A few studies have reported the anti-inflammatory effects of enrofloxacin. In this study, we used mouse spleen cells treated with lipopolysaccharide (LPS) and examined the effects of enrofloxacin. Several assays were performed in LPS-treated spleen cells after the enrofloxacin treatment. Enrofloxacin inhibited the metabolic activity and mitochondrial membrane potential of LPS-treated spleen cells significantly. On the other hand, enrofloxacin did not alter the proportion of the subsets in spleen cells, and did not induce cell death. The production of tumor necrosis factor-alpha in LPS-treated spleen cells was inhibited by enrofloxacin. Overall, enrofloxacin had modulatory activity in spleen cells treated with LPS. These data may broaden the use of enrofloxacin as an antibiotic with anti-inflammatory activity in veterinary clinics.

• Restorative Dentistry and Endodontics
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• v.24 no.3
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• pp.437-446
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• 1999

Porphyromonas endodontalis(P. endodontalis) is one of the important causative bacteria of pulpal and periapical disease. P. endodontalis has lipopolysaccharide(LPS) and it plays a major role in stimulating the synthesis and release of cytokines from immune cells and prostaglandin $E_2$ from host cells. The purpose of this study is to prepare LPS from P. endodontalis and to evaluate the effect of LPS on membrane permeability of fibroblast. P. endodontalis ATCC 35406 was cultured in anaerobic condition, and LPS was extracted. LPS was confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Human periodontal ligament cell, colon fibroblast(CCD-18Co, KCLB 21459) and skin fibroblast(Detroit 551, KCLB 10110) were perfused with 0.01% P. endodontalis LPS solution, high concentration of $K^+$ solution and $Ca^{2+}$-free solution, $Ca^{2+}$ concentration ratio was measured by microfluorometry. 1. Intracellular $Ca^{2+}$ concentration was not changed in human periodontal fibroblast and skin fibroblast(Detroit 551) stimulated by P. endodontalis LPS. 2. Intracellular $Ca^{2+}$ concentration was increased in colon fibroblast(CCD-18Co) stimulated by P. endodontalis LPS. 3. Colon fibroblast(CCD-18Co) has voltage dependent $Ca^{2+}$ channel activated by high concentration of $K^+$ solution. 4. P. endodontalis LPS has no effect on the increase of intracellular $Ca^{2+}$ concentration during perfusion of $Ca^{2+}$-free solution.

• The Journal of Internal Korean Medicine
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• v.32 no.2
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• pp.203-216
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• 2011

Objectives : This study was conducted to evaluate the protective effects of bee venom on lipopolysaccharide (LPS)-induced chronic obstructive pulmonary disease (COPD). Methods : In this study, LPS was administrated to Balb/c mice to induce a disease that resembles COPD. 2 hr prior to LPS administration, mice were treated with bee venom via an intraperitoneal injection. Total cell number and neutrophils number in bronchoalveolar lavage fluid were counted and pro-inflammatory cytokines were also measured. For histologic analysis, periodic acid Schiff (PAS) and hematoxylin and eosin (H&E) stains were evaluated. Proliferating cell nuclear antigens (PCNA) were also assessed by immunohistochemistry. Results : On 7 days after LPS stimulation, influx of neutrophils significantly decreased in the bee venom group, compared with the COPD group. In addition, TNF-a and IL-6 levels decreased in bee venom group. Histological results also demonstrated the attenuation effect of bee venom on LPS-induced lung inflammation. Conclusions : These data suggest that bee venom has protective effects on LPS-induced lung inflammation. Therefore, bee venom may represent a novel therapeutic agent for lung inflammation and in particular for COPD.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.6
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• pp.593-600
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• 2014

This study is aimed to investigate the anti-inflammatory effect of Euphorbiae kansui radix methanol extract (ERE) in lipopolysaccharide(LPS)-stimulated mouse peritoneal macrophages. Peritoneal macrophages were obtained from thioglycollate-injected Balb/c mice. Cells were stimulated with LPS or LPS plus interferon-gamma (IFN-${\gamma}$) in the presence of ERE and various inflammatory markers were assayed. Finally, LPS-induced signaling molecules were measured. ERE up to $400{\mu}g/m{\ell}$, was not cytotoxic to ERE inhibited LPS/IFN-${\gamma}$-induced nitric oxide (NO), inducible NO synthase. ERE also reduced the levels of cyclooxygenase-2 and the proinflammatory cytokines such as tumor necrosis factor-${\alpha}$, interleukin(IL)-6 and IL-12. The inhibitory effect of ERE on LPS-induced $I{\kappa}B{\alpha}$ degradation was weak but phosphorylation of JNK, p38 and ERK1/2 was strongly suppressed. Our data indicated that the anti-inflammatory effect of ERE in LPS-stimulated macrophages was partly mediated by its inhibition of JNK, p38 and ERK1/2.

• Development and Reproduction
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• v.20 no.2
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• pp.91-99
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• 2016

Lipopolysaccharide (LPS), an endotoxin, elicits strong immune responses in mammals. Several lines of evidence demonstrate that LPS challenge profoundly affects female reproductive function. For example, LPS exposure affects steroidogenesis and folliculogenesis, resulting in delayed puberty onset. The present study was conducted to clarify the mechanism underlying the adverse effect of LPS on the delayed puberty in female rats. LPS was daily injected for 5 days ($50{\mu}g/kg$, PND 25-29) to treated animals and the date at VO was evaluated through daily visual examination. At PND 39, animals were sacrificed, and the tissues were immediately removed and weighed. Among the reproductive organs, the weights of the ovaries and oviduct from LPS-treated animals were significantly lower than those of control animals. There were no changes in the weights of uterus and vagina between the LPS-treated and their control animals. immunological challenge by LPS delayed VO. Multiple corpora lutea were found in the control ovaries, indicating ovulations were occurred. However, none of corpus luteum was present in the LPS-treated ovary. The transcription level of steroidogenic acute regulatory protein (StAR), CYP11A1, CYP17A1 and CYP19 were significantly increased by LPS treatment. On the other hand, the levels of $3{\beta}$-HSD, $17{\beta}$-HSD and LH receptor were not changed by LPS challenge. In conclusion, the present study demonstrated that the repeated LPS exposure during the prepubertal period could induce multiple alterations in the steroidogenic machinery in ovary, and in turn, delayed puberty onset. The prepubertal LPS challenge model used in our study is useful to understand the reciprocal regulation of immune (stress) - reproductive function in early life.

• The Korea Journal of Herbology
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• v.24 no.3
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• pp.79-86
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• 2009

Objectives : The present study investigated Inflammatory effect of Coptidis Rhizoma in lipopolysaccharideexposed rats and Raw 264.7 cells. Methods： The plasma concentration of IL-1$\beta$, IL-6 and TNF-$\alpha$ peaked at 5 h after LPS injection, and the values of the Coptidis Rhizoma extract groups were lower than those of the control group. In the increment of cytokines concentration at 2 h and 5 h after LPS injection, the Coptidis Rhizoma groups were lower than that of control group. The plasma concentration of IL-10 peaked at 5 h after LPS injection, and the values of the Coptidis Rhizoma extract groups were higher than those of the control group. In the increment of cytokines concentration at 2 h and 5 h after LPS injection, the Coptidis Rhizoma groups were higher than that of control group. Liver cytokines measurement was done at 5 h after LPS injection. The concentration of liver IL-1$\beta$ and IL-6 in the Coptidis Rhizoma groups was lower than that of the control group. The concentrations of liver TNF-$\alpha$, and IL-10 showed no significant differences among all the treatment groups. Results： In the studies of lipopolysaccharide-exposed Raw 264.7 cells, the concentration of IL-1$\beta$, IL-6 and TNF-$\alpha$ in the lipopolysaccharide-exposed cells groups was higher than that of control group (normal group), and in the lipopolysaccharide-exposed cells groups, these values showed a tendency to decrease in the Coptidis Rhizoma groups. The concentration of IL-10 in the lipopolysaccharide-exposed cells groups was higher than that of control group (normal group), and in the lipopolysaccharide-exposed cells groups, the values showed a tendency to increase in the Coptidis Rhizoma groups. Conclusions： These results indicate that the Coptidis Rhizoma extracts have an functional material for Inflammatory activities.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.12
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• pp.1667-1675
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• 2009

This study was conducted to determine whether L-arginine (Arg) supplementation could improve intestinal function in weaned pigs after an Escherichia coli lipopolysaccharide (LPS) challenge. Treatments included: i) non-challenged control (CONTR, pigs fed a control diet and injected with sterile saline); ii) LPS-challenged control (LPS, pigs fed the same control diet and challenged by injection with Escherichia coli LPS); iii) LPS+0.5% Arg (pigs fed a 0.5% Arg diet and challenged with LPS); and iv) LPS+1.0% Arg (pigs fed a 1.0% Arg diet and challenged with LPS). On d 16, pigs were administrated with LPS or sterile saline. D-xylose was orally administrated at 2 h following LPS challenge, and blood samples were collected at 3 h following LPS challenge. At 6 h post-challenge, pigs were sacrificed and intestinal mucosa samples were collected. Supplementation of Arg attenuated LPS-induced damage in gut digestive and barrier functions, as indicated by an increase in ileal lactase activity, and duodenal and ileal diamine oxidase activities (p<0.05). Arg administration also prevented the increase of jejunal malondialdehyde content and the decrease of ileal superoxide dismutase activity by LPS challenge (p<0.05). Furthermore, the jejunal nitric oxide level and inducible nitric oxide synthase activity were also improved after Arg supplementation (p<0.05). These results indicate that Arg supplementation has beneficial effects in alleviating the impairment of gut function induced by LPS challenge.

• Journal of Periodontal and Implant Science
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• v.35 no.3
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• pp.675-685
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• 2005

Bone resorption involves sequential stages of osteoclast precursor migration and differentiation of osteoclast precursors into multinucleated osteoclasts. Stromal cell derived factor (SDF)-1 is a chemotactic factor for osteoclast precursor migration. Matrix metalloproteinase (MMP)-9 is involved in migration of osteoclast precursors and activation of $interleukin(IL)-1{\beta}$. Alveolar bone destruction is a characteristic feature of periodontal disease. Treponema lecithinolyticum is a oral spirochete isolated from the periodontal lesions. The effect of lipopolysaccharide(LPS) from T. lecithinolyticum on expression of SDF-1 and MMP-9 was examined in cocultures of bone marrow cells and osteblasts derived from mouse calvariae. T. lecithinolyticum LPS increased expression of MMP-9 in the coculture. Polymyxin B, an inhibitor of LPS, abolished the increase of MMP-9 mRNA expression by LPS. LPS did not increase the expression of SDF-1, $IL-1{\beta}$ and tumor necrosis $factor(TNF)-{\alpha}$ mRNA in cocultures. Prostaglandin $E_2(PGE_2)$ up-regulated the expression of MMP-9 and NS398, an inhibitor of $PGE_2$ synthesis, down-regulated the induction of MMP-9 expression by T. lecitbinolyticm LPS. These results suggest that T. lecitbinolyticm LPS increases MMP-9 expression in bone cells via $PGE_2$ and that the induction of MMP-9 expression by T. lecitbinolyticm LPS is involved in alveolar bone destruction of periodontitis patients by the increase of osteoclast precursor migration and the activation of bone resorption-inducing cytokine.