scholarly journals Effect of Bee Venom Pharmacopuncture on Inflammation in Mouse Model of Induced Atopic Dermatitis

2020 ◽  
Vol 37 (2) ◽  
pp. 123-127
Author(s):  
Kyeong Ju Park ◽  
Ho-Sueb Song

Background: This study was designed using a mouse model of atopic dermatitis [phthalic anhydride (PA)-treated mice], to investigate the anti-inflammatory effect of bee venom pharmacopuncture (BVP) in keratinocytes.Methods: Western blot analysis was performed to investigate inflammation related protein expression of iNOS, COX-2, phospho-ERK (p-ERK), and ERK, in LPS (1 μg/mL)-activated keratinocytes, following BVP treatment, and in PA-treated mice, after BVP treatment. Griess reaction was performed to investigate NO concentration. Enzyme-linked immunosorbent assays were used to determine the concentrations of interleukin (IL)-4+, IL-17A+, IL-13 and IL-4 in PA-treated mice after BVP treatment. In addition, monocyte, macrophage, neutrophil, and eosinophil counts were measured to observe the changes in white blood cell infiltration.Results: The keratinocytes of the BVP-treated group showed a decreased expression of iNOS, COX-2, ERK at 5 OX-2, ERK E, and p-ERK at 1, 2 and 5 RKRK ERK ERK, and a dose-dependent decrease in NO concentration at 2 and 5 ntrationof s. In the BVP-treated groups (0.1 μ.1-trea μ.1-treated gr), PA-treated mice showed recovery after 4 weeks which was dose-dependent, showing a significant decrease in clinical scores for AD, and a decreased concentration of IL-13 and IL-4 with BV treatment. There was a dose-dependent decrease in the infiltration of eosinophils, neutrophils, monocytes, macrophages, and a decreased thickness of the epidermis due to inflammation, and decreased expressions of iNOS, COX-2, p-ERK, ERK, especially in the 0.1 μ0/mL BVP-treated group,<br>Conclusion: These results suggest that BVP may be an effective alternative treatment for atopic dermatitis.

2021 ◽  
Author(s):  
Madison Feng ◽  
Sara Mata Lopez ◽  
Soraya Manaviazar ◽  
Hamish A. Watson ◽  
Karl Hale ◽  
...  

<p>(-)-Agelastatin A (AA) in 1,2-propanediol (3-deoxy-DL-glycerol) elicits a dose-dependent decrease in OPN mRNA expression in canine Duchenne Muscular Dystrophy (DMD) myoblasts at doses ranging from 0.01 nM-30 nM. When intraperitoneally administered in the same vehicle to mdx mice at 2.5 mg/kg/day for two weeks, and at 1.5 mg/kg/day twice-weekly for two weeks, (-)-AA brings about a significant decrease in exercise-induced muscle damage through its attenuation of OPN expression. Because (-)-AA is known to downregulate OPN, this study confirms that the use of small molecule OPN downregulatory drugs can beneficially modify the phenotype in DMD animal models and potentially affected boys</p>


2007 ◽  
Vol 292 (1) ◽  
pp. G409-G418 ◽  
Author(s):  
Ping Cong ◽  
Zuo-Liang Xiao ◽  
Piero Biancani ◽  
Jose Behar

The gallbladder (GB) maintains tonic contraction modulated by neurohormonal inputs but generated by myogenic mechanisms. The aim of these studies was to examine the role of prostaglandins in the genesis of GB myogenic tension. Muscle strips and cells were treated with prostaglandin agonists, antagonists, cyclooxygenase (COX) inhibitors, and small interference RNA (siRNA). The results show that PGE2, thromboxane A2 (TxA2), and PGF2α cause a dose-dependent contraction of muscle strips and cells. However, only TxA2 and PGE2 (E prostanoid 1 receptor type) antagonists induced a dose-dependent decrease in tonic tension. A COX-1 inhibitor decreased partially the tonic contraction and TxB2 (TxA2 stable metabolite) levels; a COX-2 inhibitor lowered the tonic contraction partially and reduced PGE2 levels. Both inhibitors and the nonselective COX inhibitor indomethacin abolished the tonic contraction. Transfection of human GB muscle strips with COX-1 siRNA partially lowered the tonic contraction and reduced COX-1 protein expression and TxB2 levels; COX-2 siRNA also partially reduced the tonic contraction, the protein expression of COX-2, and PGE2. Stretching muscle strips by 1, 2, 3, and 4 g increased the active tension, TxB2, and PGE2 levels; a COX-1 inhibitor prevented the increase in tension and TxB2; and a COX-2 inhibitor inhibited the expected rise in tonic contraction and PGE2. Indomethacin blocked the rise in tension and TxB2 and PGE2 levels. We conclude that PGE2 generated by COX-2 and TxA2 generated by COX-1 contributes to the maintenance of GB tonic contraction and that variations in tonic contraction are associated with concomitant changes in PGE2 and TxA2 levels.


2018 ◽  
Vol 8 (5) ◽  
pp. 354-357
Author(s):  
M. Swapna Reddy ◽  
B. Ramya Kuber

Objective: To evaluate antiplasmodial activity of Caesalpinia crista seed extracts Methods:  Antiplasmodial activity of the seed extracts of Caesalpinia crista against rodent malaria infections in chloroquine sensitive Plasmodium falcipuram strain was investigated, and oral acute toxicity of seed extracts of Caesalpinia crista was also evaluated. Results: The findings of this study revealed significant (P < 0.05) and dose dependent decrease in parasitaemia in the parasitized groups treated with varying doses of the extract (50-200 mg/kg p.o.) in both suppressive and curative tests. There was also significant decrease in parasitaemia density in the chloroquine treated group. The alcoholic extract was found no toxicity in wistar rats and the oral LD50 was determined to be greater than 5000 mg/kg. Conclusion: Seed extracts of Caesalpinia crista extract possesses potent antiplasmodial activity and may therefore, serve as potential sources of new antimalarial agents Keywords: Plasmodium falcipuram, Caesalpinia crista, Plant extracts, Phytochemicals, Toxicity tests, malaria.


2021 ◽  
Author(s):  
Madison Feng ◽  
Sara Mata Lopez ◽  
Soraya Manaviazar ◽  
Hamish A. Watson ◽  
Karl Hale ◽  
...  

<p>(-)-Agelastatin A (AA) in 1,2-propanediol (3-deoxy-DL-glycerol) elicits a dose-dependent decrease in OPN mRNA expression in canine Duchenne Muscular Dystrophy (DMD) myoblasts at doses ranging from 0.01 nM-30 nM. When intraperitoneally administered in the same vehicle to mdx mice at 2.5 mg/kg/day for two weeks, and at 1.5 mg/kg/day twice-weekly for two weeks, (-)-AA brings about a significant decrease in exercise-induced muscle damage through its attenuation of OPN expression. Because (-)-AA is known to downregulate OPN, this study confirms that the use of small molecule OPN downregulatory drugs can beneficially modify the phenotype in DMD animal models and potentially affected boys</p>


2019 ◽  
Vol 28 (1) ◽  
pp. 253-263 ◽  
Author(s):  
Yu Jin Lee ◽  
Myung Jin Oh ◽  
Dong Hun Lee ◽  
Yong Sun Lee ◽  
Jiin Lee ◽  
...  

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1357-1357
Author(s):  
Hye-Ja Lee ◽  
Hung-The Dang ◽  
Gyeoung-Jin Kang ◽  
Jee H Jung ◽  
Hee-Kyoung Kang ◽  
...  

Abstract Abstract 1357 Poster Board I-380 Jasmonic acid and methyl jasmonate are fatty acid-derived cyclopentanones, found in the plants, and play major roles in a defense against insects and disease. Methyl jasmonate suppresses cellular proliferation and induces apoptosis in human and mouse cancer cell lines. Methyl jasmonate increased the life span of EL-4 lymphoma-bearing mice with selective cytotoxicity against lymphoma cells while sparing normal blood lymphocytes. Inflammation is one of the defence mechanisms against pathogens, caused by diverse microbial products. Microbial products are detected by the Toll-like receptors (TLRs) that are expressed at high levels on macrophages and dendritic cells. The complex of the TLRs and their ligand initiates a wide spectrum of responses from phagocytosis to production of a variety of cytokines, which enhance the inflammatory and adaptive immune responses. Of these TLRs, TLR4 recognizes the product of gram-negative bacteria, LPS. LPS stimulated-cells produce inflammatory cytokines (TNF-α and IL-6), and inducible enzymes of iNOS and COX-2. Recent evidence reveal that some microRNAs (miRNAs) play important roles in inflammation; miRNA-146a plays central roles in the negative feedback regulation of IL-1b-induced inflammation and miR-155 enhances the release of inflammatory mediators during the innate immune responses. Our structural analysis shows that methyl jasmonate contains enone group which is a common functional moiety in anti-inflammatory drugs. Our previous works found that methyl jasmonate has anti-inflammatory effects and the related compound methyl dehydro-jasmonate (J2) had the highest anti-inflammatory effect in lipopolysaccharide (LPS)-activated RAW264.7 murine macrophage cells of all synthesized methyl jasmonate analogues. In this study, we wanted to elucidate molecular targets of J2 action in its anti-inflammatory properties. We observed that a LPS stimulation of RAW264.7 cell line also induced known inflammatory markers; TNF-α, IL-6, iNOS and COX-2. Our analysis of miRNAs changes revealed an increase of miR-155 (>8 fold) and miR-146a (>3 fold), but not miR-125b. In a J2 toxicity test on the LPS stimulated RAW264.7 cells, the J2 treatment protected LPS treated RAW264.7 cells starting at 6.25 μM. We then tested J2 effects on various mediators of inflammation. We found that J2 suppressed inductions of TNF-α, IL-6, iNOS and COX-2 at a transcript level in a dose-dependent manner (IC50 = 18∼25 μM) and confirmed it also at a protein level for iNOS and COX-2. We then found that miR-155 induction was inhibited by J2 dose-dependent manner, J2 suppressed miR-146a only at 50 μM. The NF-kB pathway and MAPK pathway are thought to be important mediators of LPS induced inflammation and we show that J2 had significant effects on NF-kB, p65, and IkB while no or minimal effect on JNK, p38, and ERK. In conclusion, the present study demonstrates that J2 supressed LPS stimulation in RAW264.7 cells and it targets miR-155, and NF-kB pathway. In addition, our results also suggest that MAPK pathway may not contribute to the induction of inflammatory markers (i.e. TNF-α, IL-6, iNOS, and COX-2). Disclosures No relevant conflicts of interest to declare.


Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 3058
Author(s):  
Takeshi Yoshimi ◽  
Yoshiaki Yamagishi ◽  
Issei Kanegawa ◽  
Megumi Suda ◽  
Rei Saiki ◽  
...  

We investigated the effects of enteral nutrition formula on non-steroidal anti-inflammatory drug (NSAID)-induced gastric lesions in mice. Male ICR mice aged 7–9 weeks old were fasted, then orally given either purified water, Mermed® One, or 2-fold diluted Terumeal® 2.0α as enteral nutrition (25 or 50 mL/kg each). Indomethacin (IND) was orally administered at 20 mg/kg after 30 min, and the stomach was removed 6 h later and fixed in formalin. The number and area of lesions in the stomachs of the mice given enteral nutrition showed a significant, dose-dependent decrease compared to the purified water-treated group, and no significant difference was seen between the two enteral nutrition-treated groups. Comparable time courses of plasma IND concentrations suggest that enteral nutrition does not inhibit gastrointestinal absorption of IND. Our findings indicate that administering enteral nutrition could inhibit the onset of NSAID-induced gastric ulcers.


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