scholarly journals Ameliorative Effect of Heat-Killed Lactobacillus plantarum L.137 and/or Aloe vera against Colitis in Mice

Processes ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 225
Author(s):  
Heba Ismaeil ◽  
Walied Abdo ◽  
Said Amer ◽  
Amin Tahoun ◽  
Diaa Massoud ◽  
...  
Keyword(s):  
Lactobacillus Plantarum ◽  
Nuclear Factor Kappa B ◽  
Aloe Vera ◽  
Tnf Α ◽  
Ameliorative Effect ◽  
Inflammatory Bowel ◽  
Oxide Synthase ◽  
High Histologic Grade ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Inflammatory bowel disease (IBD) is one of the predominant intestinal diseases associated with chronic inflammation and ulceration of the colon. This study explored the ameliorative effect of Aloe vera extract (Aloe) and/or heat-killed Lactobacillus plantarum L.137 (HK L.137) on dextran sodium sulfate (DSS)-induced colitis in mice. Aloe and/or HK L.137 were supplied for 9 days and the mice were challenged with DSS for 7 days. The DSS group demonstrated bloody diarrhea, colitis of high histologic grade, increased nuclear factor-kappa B (NF-κB) p65, inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO), interleukin (IL)-6, and tumor necrosis factor (TNF)-α, and decreased IL-10 expression. These alterations were dwindled in DSS-induced mice treated with Aloe and HK L.137 separately. Aloe and HK L.137 together have augmented the therapeutic effect of each other. In conclusion, our findings demonstrated that Aloe and/or HK L.137 ameliorated DSS-induced colitis by promoting the secretion of anti-inflammatory cytokines and suppressing pro-inflammatory mediators. This study indicated that A. vera may function synergistically with HK L.137 to confer an effective strategy to prevent colitis.

scholarly journals Immunogenicity and Protection Induced by a Mycobacterium tuberculosissigE Mutant in a BALB/c Mouse Model of Progressive Pulmonary Tuberculosis

2010 ◽  
Vol 78 (7) ◽  
pp. 3168-3176 ◽  
Author(s):  
Rogelio Hernandez Pando ◽  
Leon Diana Aguilar ◽  
Issar Smith ◽  
Riccardo Manganelli
Keyword(s):  
Mutant Strain ◽  
Virulent Strain ◽  
Survival Rates ◽  
Live Vaccine ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

ABSTRACT Tuberculosis is still one of the main challenges to human global health, leading to about two million deaths every year. One of the reasons for its success is the lack of efficacy of the widely used vaccine Mycobacterium bovis BCG. In this article, we analyze the potential use of an attenuated mutant of Mycobacterium tuberculosis H37Rv lacking the sigma factor σE as a live vaccine. We have demonstrated that BALB/c mice infected by the intratracheal route with this mutant strain showed significantly higher survival rates and less tissue damage than animals infected with the parental or complemented mutant strain. Although animals infected with the sigE mutant had low bacillary loads, their lungs showed significantly higher production of the protective factors gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), and β-defensins than those of animals infected with the parental or complemented mutant strain. Moreover, we demonstrate that the sigE mutant, when inoculated subcutaneously, was more attenuated than BCG in immunodeficient nude mice, thus representing a good candidate for a novel attenuated live vaccine strain. Finally, when we used the sigE mutant as a subcutaneous vaccine, it was able to induce a higher level of protection than did BCG with both H37Rv and a highly virulent strain of M. tuberculosis (Beijing code 9501000). Taken together, our findings suggest that the sigE mutant is a very promising strain for the development of a new vaccine against tuberculosis.

scholarly journals Curcumin protects liver inflammation by suppressing expression of inducible nitric oxide synthase in primary cultured rat hepatocytes

2017 ◽  
Vol 7 (9) ◽  
pp. 716 ◽  
Author(s):  
Richi Nakatake ◽  
Hidehiko Hishikawa ◽  
Hideyuki Matushima ◽  
Yusuke Nakamura ◽  
Morihiko Ishizaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Rat Hepatocytes ◽  
No Production ◽  
Type I ◽  
Tnf Α ◽  
Cultured Rat Hepatocytes ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Background: Curcumin has beneficial effects on organ metabolism. However, there is little evidence that curcumin affects inflammatory mediators, such as tumor necrosis factor (TNF)-α and nitric oxide (NO). In an inflamed liver, proinflammatory cytokines stimulate liver cells, followed by the induction of inducible NO synthase (iNOS). Excessive NO produced by iNOS is one of the factors in liver injury. Therefore, inhibiting iNOS induction for preventing liver injury is important.Objective: This study aimed to investigate liver protective effects of curcumin by examining interleukin (IL)-1β-stimulated hepatocytes.Methods: Primary cultured rat hepatocytes were treated with IL-1β in the presence or absence of curcumin. Induction of NO production and iNOS, and the signaling pathway of iNOS were analyzed.Results: Simultaneous addition of IL-1β and curcumin decreased expression levels of iNOS protein and mRNA, resulting in inhibition of NO production. Curcumin also reduced mRNA expression of TNF-α and IL-6. Curcumin inhibited two essential signaling pathways for iNOS induction, NF-κB activation and type I IL-1 receptor upregulation. Transfection experiments revealed that curcumin reduced iNOS mRNA levels at the promoter activation and mRNA stabilization steps. Delayed administration of curcumin after IL-1β addition also inhibited iNOS induction.Conclusions: Curcumin affects induction of inflammatory mediators, such as iNOS and TNF-α, in part through the inhibition of NF-κB activation in hepatocytes. Curcumin may have therapeutic potential for organ injuries, including the liver.Key words: curcumin, inducible nitric oxide synthase, liver injury, primary cultured hepatocytes, nuclear factor-κB, type I interleukin-1 receptor, tumor necrosis factor-α. 

scholarly journals Glutathione inhibits expression of the proinflammatory biomarker inducible nitric oxide synthase in hepatocytes

2018 ◽  
Vol 8 (12) ◽  
pp. 544
Author(s):  
Richi Nakatake ◽  
Masaya Kotsuka ◽  
Yuki Hashimoto ◽  
Masahiko Hatta ◽  
Morihiko Ishizaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Liver Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Type I ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide ◽  
Inos Induction

Background: Intracellular glutathione (GSH) plays an important regulatory role in the host response to liver injury. However, there have been few scientific reports on the anti-inflammatory effects of GSH. In the inflamed liver, proinflammatory cytokines stimulate liver cells, followed by expression of inducible nitric oxide synthase (iNOS). Excessive nitric oxide (NO) levels produced by iNOS are one of the factors involved in liver injury. Therefore, inhibiting iNOS induction is important for preventing liver injury. This study aimed to investigate the protective effects of GSH on the liver by examining interleukin (IL)-1β-stimulated hepatocytes.Methods: Primary cultured rat hepatocytes were treated with IL-1β in the presence or absence of GSH. Induction of iNOS and its signaling pathway were analyzed.Results: Addition of GSH decreased IL-1β-induced iNOS protein and mRNA expression levels, which resulted in inhibition of NO production. GSH also decreased tumor necrosis factor (TNF)-α and IL-6 mRNA expression. GSH blocked “type I IL-1 receptor upregulation”, one of the essential signaling pathways for iNOS induction, through inactivation of an upstream kinase, phosphatidylinositol 3-kinase/Akt. In contrast, GSH had no effects on degradation of IκB and activation of NF-ĸB (nuclear translocation and its DNA binding). Transfection experiments revealed that GSH reduced iNOS mRNA levels at the promoter transactivation and mRNA stabilization steps. Delayed administration of GSH after IL-1β addition also inhibited iNOS induction. Conclusions: Our study suggests that GSH affects induction of inflammatory mediators, including iNOS and TNF-α, indicating its therapeutic potential for organ injuries, especially for the liver.Keywords: glutathione, inducible nitric oxide synthase, liver injury, primary cultured hepatocytes, type I interleukin-1 receptor, tumor necrosis factor-α

scholarly journals Aktivitas Imunomodulator Ekstrak Metanol dan Fraksi buah Talok (Muntingia calabura L.) pada Sel RAW 264.7

2021 ◽  
Vol 6 (2) ◽  
pp. 82
Author(s):  
Tanti Azizah Sujono ◽  
Ika Trisharyanti Dian Kusumowati ◽  
Rima Munawaroh
Keyword(s):  
Tumor Necrosis ◽  
Raw 264.7 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Reverse Transcription Pcr ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Muntingia Calabura ◽  
Inducible Nitric Oxide

<p>Buah talok (<em>Muntingia</em><em> calabura</em> L) secara empiris telah diketahui mempunyai banyak manfaat bagi kesehatan, diantaranya adalah sebagai imunomodulator. Namun mekanisme aksinya sebagai imunomodulator belum diketahui secara pasti. Penelitian ini bertujuan untuk mengevaluasi efek imunomodulator ekstrak metanolik dan fraksi buah talok pada sel makrofag RAW 264.7. Sel RAW 264.7 diberi perlakuan dengan ekstrak metanolik buah talok (EMBT), fraksi heksan buah talok (FHBT), fraksi diklorometana buah talok (FDBT), fraksi etil asetat buah talok (FEABT) serta kelompok kontrol sel (KS), kontrol lipopolisakarida (LPS) dan deksametason. Viabilitas sel diukur dengan metode <em>MTT</em> <em>assay</em> dilanjutkan isolasi RNA, pembuatan cDNA dan PCR. Level ekspresi mRNA dari gen-gen seperti toll like receptor 4 (TLR4), interferon (IFN)-ɣ, interleukin (IL)-6, inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α pada sel RAW 264.7 yang diinduksi lipopolisakarida (LPS) dianalisis dengan metode reverse transcription-PCR. Hasil penelitian menunjukkan bahwa deksametason menghambat ekspresi iNOS, IL-6, TNF-α, TLR4, IFN- ɣ dan NF-kB dibandingkan dengan kontrol sel dan LPS. Hal ini mengindikasikan bahwa deksametason mempunyai aktivitas antiinflamasi. Ekstrak metanolik (EMBT) dan fraksi buah talok (FHBT, FDBT dan FEABT) menurunkan ekspresi gen iNOS, TNF-α, IL-6, IFN- ɣ dan NF-kB jika dibandingkan dengan kontrol sel dan LPS, hal ini menunjukkan adanya aktivitas antiinflamasi. Ekstrak metanolik dan fraksi buah talok mempunyai  aktivitas imunomodulator melalui penghambatan inflamasi dengan menurunkan ekspresi gen iNOS, TNF-α, IL-6, IFN- ɣ dan NF-kB pada sel RAW 264.7 yang diinduksi LPS. </p>

scholarly journals Bioactive Diterpenes, Norditerpenes, and Sesquiterpenes from a Formosan Soft Coral Cespitularia sp.

2021 ◽  
Vol 14 (12) ◽  
pp. 1252
Author(s):  
You-Cheng Lin ◽  
Chi-Chien Lin ◽  
Yi-Chia Chu ◽  
Chung-Wei Fu ◽  
Jyh-Horng Sheu
Keyword(s):  
Nitric Oxide ◽  
Soft Coral ◽  
2D Nmr ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Chemical investigation of the soft coral Cespitularia sp. led to the discovery of twelve new verticillane-type diterpenes and norditerpenes: cespitulins H–O (1–8), one cyclic diterpenoidal amide cespitulactam L (9), norditerpenes cespitulin P (10), cespitulins Q and R (11 and 12), four new sesquiterpenes: cespilins A–C (13–15) and cespitulolide (16), along with twelve known metabolites. The structures of these metabolites were established by extensive spectroscopic analyses, including 2D NMR experiments. Anti-inflammatory effects of the isolated compounds were studied by evaluating the suppression of pro-inflammatory protein tumor necrosis factor-α (TNF-α) and nitric oxide (NO) overproduction, and the inhibition of the gene expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in lipopolysaccharide-induced dendritic cells. A number of these metabolites were found to exhibit promising anti-inflammatory activities.

scholarly journals Protective effects of active hexose correlated compound in a rat model of liver injury after hepatectomy

2016 ◽  
Vol 6 (11) ◽  
pp. 702 ◽  
Author(s):  
Richi Nakatake ◽  
Yoshito Tanaka ◽  
Yosuke Ueyama ◽  
Hirokazu Miki ◽  
Morihiko Ishizaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Rat Model ◽  
Inflammatory Mediators ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Background: Recent evidence has indicated that a functional food, active hexose correlated compound (AHCC), has liver-protective effects via suppression of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF)-α.Objective: This study aimed to investigate whether AHCC has beneficial effects in a rat model of endotoxin-induced liver injury after partial hepatectomy, in addition to clarifying the mechanisms of action of AHCC.Methods: Rats were treated with 70% of partial hepatectomy and lipopolysaccharide (PH/LPS) to induce acute liver injury. A normal diet with or without 2% AHCC was administered orally 10 days before 70% hepatectomy. Inflammatory mediators were analyzed.Results: AHCC improved the survival rate by 70% in PH/LPS rats. AHCC prevented an increase in serum transaminase levels, and histopathological changes and apoptosis in the liver. AHCC reduced iNOS mRNA and protein expression in the liver, resulting in inhibition of nitric oxide production. AHCC also reduced TNF-α, cytokine-induced neutrophil chemoattractant-1, and interleukin-6 mRNA expression, but enhanced expression of interleukin-10. An electrophoretic mobility shift assay with hepatic nuclear extracts demonstrated that AHCC reduced the activation of nuclear factor (NF)-κB induced by PH/LPS treatment.Conclusion: AHCC inhibits induction of inflammatory mediators, including iNOS and TNF-α, in part through inhibition of NF-κB activation in a rat model of liver injury. Our findings suggest that AHCC prevents postoperative liver failure after liver resection.Keywords: active hexose correlated compound, inducible nitric oxide synthase, liver injury, nuclear factor-κB, tumor necrosis factor-α

Medicinal lavender modulates the enteric microbiota to protect against Citrobacter rodentium-induced colitis

2012 ◽  
Vol 303 (7) ◽  
pp. G825-G836 ◽  
Author(s):  
J. Baker ◽  
K. Brown ◽  
E. Rajendiran ◽  
A. Yip ◽  
D. DeCoffe ◽  
...  
Keyword(s):  
Severe Disease ◽  
Apical Region ◽  
Therapeutic Effects ◽  
Intestinal Epithelial ◽  
Citrobacter Rodentium ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Inflammatory bowel disease, inclusive of Crohn's disease and ulcerative colitis, consists of immunologically mediated disorders involving the microbiota in the gastrointestinal tract. Lavender oil is a traditional medicine used to relieve many gastrointestinal disorders. The goal of this study was to examine the therapeutic effects of the essential oil obtained from a novel lavender cultivar, Lavandula × intermedia cultivar Okanagan lavender (OLEO), in a mouse model of acute colitis caused by Citrobacter rodentium . In colitic mice, oral gavage with OLEO resulted in less severe disease, including decreased morbidity and mortality, reduced intestinal tissue damage, and decreased infiltration of neutrophils and macrophages, with reduced levels of TNF-α, IFN-γ, IL-22, macrophage inflammatory protein-2α, and inducible nitric oxide synthase expression. This was associated with increased levels of regulatory T cell populations compared with untreated colitic mice. Recently, we demonstrated that the composition of the enteric microbiota affects susceptibility to C. rodentium -induced colitis. Here, we found that oral administration of OLEO induced microbiota enriched with members of the phylum Firmicutes, including segmented filamentous bacteria, which are known to protect against the damaging effects of C. rodentium . Additionally, during infection, OLEO treatment promoted the maintenance of microbiota loads, with specific increases in Firmicutes bacteria and decreases in γ-Proteobacteria. We observed that Firmicutes bacteria were intimately associated with the apical region of the intestinal epithelial cells during infection, suggesting that their protective effect was through contact with the gut wall. Finally, we show that OLEO inhibited C. rodentium growth and adherence to Caco-2 cells, primarily through the activities of 1,8-cineole and borneol. These results indicate that while OLEO promoted Firmicutes populations, it also controlled pathogen load through antimicrobial activity. Overall, our results reveal that OLEO can protect against colitis through the microbial-immunity nexus and that a pharmacological agent, in this case OLEO, alters the normal enteric microbiota.

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