Protective effect of Astragali radix extract on interleukin 1?-induced in?ammation in human amnion

2003 ◽  
Vol 17 (9) ◽  
pp. 1016-1020 ◽  
Author(s):  
Yun-Hee Shon ◽  
Kyung-Soo Nam
Keyword(s):  
Protective Effect ◽  
Interleukin 1 ◽  
Human Amnion ◽  
Astragali Radix

scholarly journals Anti-Amnesic Effect of Walnut via the Regulation of BBB Function and Neuro-Inflammation in Aβ1-42-Induced Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 976
Author(s):  
Jong Min Kim ◽  
Uk Lee ◽  
Jin Yong Kang ◽  
Seon Kyeong Park ◽  
Eun Jin Shin ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Protective Effect ◽  
Tumor Necrosis ◽  
Juglans Regia ◽  
Interleukin 1 ◽  
Tumor Necrosis Factor Receptor ◽  
Heme Oxygenase 1 ◽  
Necrosis Factor Alpha ◽  
Amnesic Effect ◽  
Necrosis Factor

This study was conducted to assess the protective effect of walnut (Juglans regia L.) extract on amyloid beta (Aβ)1-42-induced institute of cancer research (ICR) mice. By conducting a Y-maze, passive avoidance, and Morris water maze tests with amyloidogenic mice, it was found that walnut extract ameliorated behavioral dysfunction and memory deficit. The walnut extract showed a protective effect on the antioxidant system and cholinergic system by regulating malondialdehyde (MDA) levels, superoxide dismutase (SOD) contents, reduced glutathione (GSH) contents, acetylcholine (ACh) levels, acetylcholinesterase (AChE) activity, and protein expression of AChE and choline acetyltransferase (ChAT). Furthermore, the walnut extract suppressed Aβ-induced abnormality of mitochondrial function by ameliorating reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and ATP contents. Finally, the walnut extract regulated the expression of zonula occludens-1 (ZO-1) and occludin concerned with blood–brain barrier (BBB) function, expression of tumor necrosis factor-alpha (TNF-α), tumor necrosis factor receptor 1 (TNFR1), phosphorylated c-Jun N-terminal kinase (p-JNK), phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (p-IκB), cyclooxygenase-2 (COX-2), and interleukin 1 beta (IL-1β), related to neuroinflammation and the expression of phosphorylated protein kinase B (p-Akt), caspase-3, hyperphosphorylation of tau (p-tau), and heme oxygenase-1 (HO-1), associated with the Aβ-related Akt pathway.

scholarly journals Possible Protective Effect of Diacerein on Doxorubicin-Induced Nephrotoxicity in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Marwa M. M. Refaie ◽  
Entesar F. Amin ◽  
Nashwa F. El-Tahawy ◽  
Aly M. Abdelrahman
Keyword(s):  
Protective Effect ◽  
Low Dose ◽  
Caspase 3 ◽  
Interleukin 1 ◽  
Treated Group ◽  
Limiting Factors ◽  
High Dose ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Nephrotoxicity is one of the limiting factors for using doxorubicin (DOX). Interleukin 1 has major role in DOX-induced nephrotoxicity, so we investigated the effect of interleukin 1 receptor antagonist diacerein (DIA) on DOX-induced nephrotoxicity. DIA (25 and 50 mg/kg/day) was administered orally to rats for 15 days, in the presence or absence of nephrotoxicity induced by a single intraperitoneal injection of DOX (15 mg/kg) at the 11th day. We measured levels of serum urea, creatinine, renal reduced glutathione (GSH), malondialdehyde (MDA), total nitrites (NOx), catalase, and superoxide dismutase (SOD). In addition, caspase-3, tumor necrosis factor alpha (TNFα), nuclear factor kappa B (NFκB) expressions, and renal histopathology were assessed. Our results showed that DOX-induced nephrotoxicity was ameliorated or reduced by both doses of DIA, but diacerein high dose (DHD) showed more improvement than diacerein low dose (DLD). This protective effect was manifested by significant improvement in all measured parameters compared to DOX treated group by using DHD. DLD showed significant improvement of creatinine, MDA, NOx, GSH, histopathology, and immunohistochemical parameters compared to DOX treated group.

scholarly journals Immunomodulating effect of fosfomycin on gut-derived sepsis caused by Pseudomonas aeruginosa in mice.

1997 ◽  
Vol 41 (2) ◽  
pp. 308-313 ◽  
Author(s):  
T Matsumoto ◽  
K Tateda ◽  
S Miyazaki ◽  
N Furuya ◽  
A Ohno ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Survival Rate ◽  
Protective Effect ◽  
Specific Activity ◽  
Bacterial Colonization ◽  
Interleukin 1 ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Bacterial Clearance ◽  
Necrosis Factor Alpha

We evaluated the protective effect of fosfomycin (FOM) and an enantiomer of fosfomycin [FOM (+); an isomer of FOM with no bactericidal activity] on murine gut-derived sepsis caused by Pseudomonas aeruginosa. Endogenous bacteremia was induced by administering cyclophosphamide (CY) and ampicillin to specific-pathogen-free mice fed P. aeruginosa. Treatment of mice with FOM at 250 mg/kg of body weight per day twice a day after the second CY administration significantly increased the survival rate compared to that for control mice treated with saline. Treatment with FOM (+) at 20 and 100 mg/kg also significantly increased the survival rate (from 30% for control mice to 80% for treated mice). The bacterial counts in the liver and blood were both significantly lower in FOM(+)-treated mice in comparison with those in liver and blood of saline-treated control mice. FOM(+) administration affected neither the bacterial colonization in the intestinal tract nor the leukocyte counts in the peripheral blood of the mice. After intravascular inoculation of P. aeruginosa, treatment of mice with FOM (+) did not enhance bacterial clearance from the blood of mice pretreated or not enhance bacterial clearance from the blood of mice pretreated or not pretreated with CY, FOM(+) significantly suppressed tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 levels in the serum of mice after gut-derived sepsis. These results indicate that both FOM and FOM(+) have protective effects against P. aeruginosa bacteremia, despite a lack of specific activity of FOM(+), and suggest that FOM may possess immunomodulating activity and that it induces a protective effect. The protective mechanism is speculated to be that FOM modulates the vivo production of inflammatory cytokines.

Studies on the action of interleukin-1 on term human fetal membranes and decidua

1994 ◽  
Vol 72 (2) ◽  
pp. 133-139 ◽  
Author(s):  
B. Alnaif ◽  
R. J. Benzie ◽  
W. Gibb
Keyword(s):  
Preterm Labor ◽  
Interleukin 1 ◽  
Fetal Membranes ◽  
Frozen Sections ◽  
Human Amnion ◽  
Chorion Laeve ◽  
Interleukin 1Α ◽  
Low Levels ◽  
High Concentrations ◽  
Dispersed Cells

Recent studies have indicated the possible importance of cytokines in the onset of term and preterm labor. To examine this further, the effect of interleukin-1β (IL-1β), interleukin-1α (IL-1α), and interleukin-6 (IL-6) on prostaglandin output by dispersed cells from human amnion, chorion laeve, and decidua obtained at term (38–40 weeks gestation) was examined. During the first or second 24 h of culture no significant effect of these interleukins on prostaglandin output was observed. The reason for this apparent refractoriness was further investigated by studying the distribution of IL-1 receptors in frozen sections of undisrupted fetal membranes and decidua at term. Whole-tissue autoradiography indicated that receptors were present in chorion–decidua but not in amnion. By using emulsion autoradiography, IL-1 receptors were found in high concentrations in chorion laeve and were absent in amnion and at low levels in the decidua. These studies indicate that under normal circumstances in human pregnancy at term IL-1 did not stimulate prostaglandin production by dispersed cells. In the case of amnion, this may be due to the absence of receptors, and therefore it would appear that the IL-1 receptor must first be induced in this tissue before it can respond to this cytokine. Furthermore, although chorion laeve expresses the IL-1 receptor, dispersed cells from this tissue did not respond to the cytokine by increasing prostaglandin output.Key words: labor, prostaglandins, interleukin-1, interleukin-1 receptor, fetal membranes, decidua.

Interleukin-1 Receptor Antagonist (IL-1ra) Production by Human Amnion, Chorion, and Decidua

1994 ◽  
Vol 32 (1) ◽  
pp. 1-7 ◽  
Author(s):  
P.L. Fidel ◽  
R. Romero ◽  
M. Ramirez ◽  
J. Cutright ◽  
S.S. Edwin ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Human Amnion ◽  
Interleukin 1 Receptor Antagonist

scholarly journals Protective Effect of Astragali Radix by Oral Administration against Japanese Encephalitis Virus Infection in Mice.

1996 ◽  
Vol 19 (9) ◽  
pp. 1166-1169 ◽  
Author(s):  
Keiji KAJIMURA ◽  
Yasuhiro TAKAGI ◽  
Noboru UEBA ◽  
Katsuhiro YAMASAKI ◽  
Yoshikazu SAKAGAMI ◽  
...  
Keyword(s):  
Virus Infection ◽  
Oral Administration ◽  
Protective Effect ◽  
Japanese Encephalitis Virus ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Astragali Radix ◽  
Japanese Encephalitis Virus Infection

scholarly journals Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Eun Bok Baek ◽  
Jin-hyung Rho ◽  
Eunhye Jung ◽  
Chang-Seob Seo ◽  
Jin-Hee Kim ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mouse Model ◽  
Protective Effect ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Transforming Growth Factor ◽  
Airway Remodeling ◽  
Interleukin 1 ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Abstract Background Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we examined the protective effect of PJH in a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) with lipopolysaccharide (LPS). Methods Mice received CS exposure for 8 weeks and intranasal instillation of LPS on weeks 1, 3, 5 and 7. PJH (100 and 200 mg/kg) was administrated daily 1 h before CS treatment for the last 4 weeks. Results Compared with CS plus LPS-exposed mice, mice in the PJH-treated group showed significantly decreased inflammatory cells count and reduced inflammatory cytokines including interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-α) levels in broncho-alveolar lavage fluid (BALF) and lung tissue. PJH also suppressed the phosphorylation of nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) caused by CS plus LPS exposure. Furthermore, CS plus LPS induced increases in matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-β (TGF-β) expression and collagen deposition that were inhibited in PJH-treated mice. Conclusions This study demonstrates that PJH prevents respiratory inflammation and airway remodeling caused by CS with LPS exposure suggesting potential therapy for the treatment of COPD.

Protective effect of chlorpromazine against the lethality of interleukin 1 in adrenalectomized or actinomicin D-sensitized mice

1989 ◽  
Vol 165 (3) ◽  
pp. 942-946 ◽  
Author(s):  
Riccardo Bertini ◽  
Marina Bianchi ◽  
Manuela Mengozzi ◽  
Pietro Ghezzi
Keyword(s):  
Protective Effect ◽  
Interleukin 1

scholarly journals Effect of Astragali Radix Extract on Lipopolysaccharide-Induced Inflammation in Human Amnion

2002 ◽  
Vol 25 (1) ◽  
pp. 77-80 ◽  
Author(s):  
Yun-Hee Shon ◽  
Jong-Ho Kim ◽  
Kyung-Soo Nam
Keyword(s):  
Human Amnion ◽  
Astragali Radix

scholarly journals Intrauterine low protein diet increases fetal beta-cell sensitivity to NO and IL-1 beta: the protective role of taurine

2001 ◽  
Vol 171 (2) ◽  
pp. 299-308 ◽  
Author(s):  
S Merezak ◽  
AA Hardikar ◽  
CS Yajnik ◽  
C Remacle ◽  
B Reusens
Keyword(s):  
Beta Cell ◽  
Protective Effect ◽  
Interleukin 1 ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Beta Alanine ◽  
Low Protein

We have demonstrated earlier that a low-protein (8% protein) diet during gestation alters fetal beta-cell development. Here, we investigated the effect of a low-protein diet as compared with a control (20% protein) diet, during gestation, on the sensitivity of fetal beta-cells against nitric oxide (NO) or interleukin-1 beta (IL-1 beta), and assessed the protective effect of taurine in vitro and in vivo. Neoformed islets from control fetuses or fetuses of dams fed a low-protein diet (LP group) were incubated with taurine, methionine or beta-alanine and then exposed to sodium nitropruside (SNP), a NO donor, or to IL-1 beta. To understand the effect of taurine in vivo, LP or control pregnant rats received 2.5% of taurine in the drinking water. Mortality and rate of apoptosis were quantified by confocal microscopy. Without treatment, rate of apoptosis was greater in LP group islets than in control islets (1.38+/-0.18% compared with 0.66+/-0.21% respectively, P<0.05). Addition of SNP 100 microM showed an augmentation in cell death, which was greater in the LP than in the control group (17.88+/-0.69% compared with 11.89+/-0.44% respectively, P<0.01). LP islets were more sensitive than control islets to IL-1 beta. Taurine was protective against SNP and IL-1 beta in both the groups, methionine provided a less protective effect than taurine, and pretreatment with beta-alanine had no protective effect. Taurine supplementation of the maternal diet reduced the rate of apoptosis induced by IL-1 beta in control islets and suppressed that induced by IL-1 beta in LP islets. Our findings indicate that a low-protein diet during gestation augments the sensitivity of fetal islet cells to NO and IL-1 beta. However, through in vitro and in vivo experiments our studies indicate that such effects can be rescued using amino acids such as taurine.

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