Diencephalic GABAergic Neurons in vitro Respond to Prolactin with a Rapid Increase in Intracellular Free Calcium

1992 ◽  
Vol 56 (2) ◽  
pp. 148-152 ◽  
Author(s):  
Walter Kolbinger ◽  
Cordian Beyer ◽  
Karl Föhr ◽  
Ingrid Reisert ◽  
Christof Pilgrim
Keyword(s):  
Gabaergic Neurons ◽  
Intracellular Free Calcium ◽  
Free Calcium

scholarly journals Rhubarb-Aconite Decoction (RAD) Drug-Containing Serum Alleviated Endotoxin-Induced Oxidative Stress Injury and Inflammatory Response in Caco-2 Cells In Vitro

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xiao-hong Du ◽  
Qing-jun Chen ◽  
Jian-bo Song ◽  
Yan Xie ◽  
Yan Zhi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Calcium Ion ◽  
Lipid Peroxide ◽  
Intestinal Injury ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Stress Injury ◽  
Oxidative Stress Injury

Rhubarb-Aconite Decoction (RAD), a famous Chinese medicine prescription, has been widely used for treating intestinal injury. However, the effect of RAD on intestinal epithelial cells is unclear. The aim of this study was to investigate the effects of RAD drug-containing serum on the oxidative stress injury and inflammatory response induced by endotoxin (ET) in Caco-2 cells in vitro. Lipid peroxide malondialdehyde (MDA), lactate dehydrogenase (LDH), caspase-11, tumor necrosis factor-α(TNF-α), interleukin-3(IL-3), and cytokeratin (CK)18, adenosine triphosphate (ATP) activity, and intracellular free calcium ion levels were measured. The results showed that ET triggered the activation of caspase-11 and the massive release of TNF-α, increased the inhibitory rate of cell growth, MDA, and LDH expressions in Caco-2 cells. Moreover, RAD drug-containing serum could inhibit caspase-11 activation, decrease the release of TNF-α and IL-3, reduce intracellular free calcium ion, and enhance CK 18 expression and ATP activity. These novel findings demonstrated that ET-induced oxidative stress injury and inflammatory response of Caco-2 cells were improved by RAD drug-containing serum, indicating that RAD may be a good choice for the treatment of intestinal injury.

Mechanism of Hyaluronic Acid Protect Rabbit Chondrocyte Apoptosis Induced by NO

2013 ◽  
Vol 295-298 ◽  
pp. 78-81
Author(s):  
Hua Liu ◽  
Hua Guang Li ◽  
Su Liu
Keyword(s):  
Hyaluronic Acid ◽  
Treated Group ◽  
Calcium Overload ◽  
Intracellular Free Calcium ◽  
Chondrocyte Apoptosis ◽  
Free Calcium ◽  
Model Group ◽  
Culture Experiment ◽  
Cell Culture Experiment

AIM: To investigate the mechanism of hyaluronic acid on rabbit chondrocyte apoptosis in vitro induced by NO. METHODS: We cultured rabbit chondrocytes as normal group and added SNP after cultured 24 h as model group. Treated group was added HA. We used cell culture experiment. We tested the activity of mitochondria though MTT. The flow cytometry detected mitochondrial membrane potential, the percentage of apoptosis and intracellular free calcium concentration.RESULTS: HA could elevate the active of chondrocyte mitochondria and MMP; it could decrease the rate of chondrocyte apoptosis and intracellular free calcium concentration.CONCLUSION: HA can inhibit the lowering of the MMP in chondrocyte, which has a stable role on MMP and inhibit apoptosis occurred. This effect may be related to inhibiting of intracellular calcium overload chondrocytes.

The effects of permeating cryoprotectants on intracellular free-calcium concentrations and developmental potential of in vitro-matured feline oocytes

2016 ◽  
Vol 28 (5) ◽  
pp. 599 ◽  
Author(s):  
Jason R. Herrick ◽  
Chunmin Wang ◽  
Zoltan Machaty
Keyword(s):  
Enzymatic Digestion ◽  
Blastocyst Stage ◽  
Intracellular Free Calcium ◽  
In Vitro Fertilisation ◽  
Free Calcium ◽  
Blastocyst Development ◽  
Oocyte Vitrification ◽  
Developmental Potential ◽  
Parthenogenetic Activation

Embryos produced from vitrified feline oocytes have resulted in pregnancies, but the efficiency of oocyte vitrification in cats is still low. Our objectives were to evaluate the effects of exposing feline oocytes to ethylene glycol (EG), propanediol (PrOH) and dimethyl sulfoxide (DMSO) on changes in intracellular free-calcium concentrations ([Ca2+]i), the time needed for enzymatic digestion of the zona pellucida (ZP), the incidence of parthenogenetic activation and degeneration and embryonic development following in vitro fertilisation (IVF). All of the chemicals tested altered [Ca2+]i, but changes in [Ca2+]i, resistance of the ZP to enzymatic digestion and the incidence of parthenogenetic activation (<5% for all treatments) were not affected (P > 0.05) by extracellular Ca2+. Exposure to EG (>44.1%) and DMSO (19.7%) increased (P < 0.05) oocyte degeneration compared with control oocytes and oocytes exposed to PrOH (≤2.5%). Following exposure to a combination of PrOH and DMSO (10% v/v each), blastocyst development (per cleaved embryo; 52.1%) was similar (P > 0.05) to control oocytes (64.4%). When oocytes were vitrified with PrOH and DMSO, 28.3% of surviving (intact plasma membrane) oocytes cleaved following IVF, but no blastocyst developed. When a non-permeating cryoprotectant (galactose, 0.25 M) was added to the vitrification medium, 47.7% of surviving oocytes cleaved and 14.3% developed to the blastocyst stage.

scholarly journals Bryophyllum pinnatum Compounds Inhibit Oxytocin-Induced Signaling Pathways in Human Myometrial Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Stefanie Santos ◽  
Leonie Zurfluh ◽  
Mónica Mennet ◽  
Olivier Potterat ◽  
Ursula von Mandach ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Calcium Concentration ◽  
Inhibitory Effect ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Myometrial Cells ◽  
Intracellular Free Calcium Concentration ◽  
Free Calcium Concentration ◽  
Bryophyllum Pinnatum

Bryophyllum pinnatum has been used in the treatment of premature labor, first in anthroposophic hospitals and, recently, in conventional settings as an add-on medication. In vitro work with hTERT human myometrial cells showed that B. pinnatum leaf press juice inhibits the increase of intracellular free calcium concentration induced by oxytocin, a hormone known to play a role in labor. Our aim was to identify fractions/compounds in B. pinnatum press juice that contribute to this inhibitory effect, and to investigate their effect on oxytocin-driven activation of the MAPK cascade. Several fractions/compounds from B. pinnatum press juice led to a concentration-dependent decrease of oxytocin-induced increase of intracellular free calcium concentration, but none of them was as strong as B. pinnatum press juice. However, the combination of a bufadienolide and a flavonoid-enriched fraction was as effective as B. pinnatum press juice, and their combination had a synergistic effect. B. pinnatum press juice inhibited oxytocin-driven activation of MAPKs SAPK/JNK and ERK1/2, an effect also exerted by the bufadienolide-enriched fraction. The effect of B. pinnatum press juice on oxytocin-induced signaling pathways was comparable to that of the oxytocin-receptor antagonist and tocolytic agent atosiban. Our findings further substantiate the use of B. pinnatum press juice preparations in the treatment of preterm labor.

Thyroid Hormone and Thyrotropin Regulate Intracellular Free Calcium Concentrations in Human Polymorphonuclear Leukocytes: In Vivo and in vitro Studies

2006 ◽  
Vol 19 (1) ◽  
pp. 205873920601900 ◽  
Author(s):  
F. Marino ◽  
L. Guasti ◽  
M. Cosentino ◽  
D. DE Piazza ◽  
C. Simoni ◽  
...  
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Differentiated Thyroid Carcinoma ◽  
Intracellular Free Calcium ◽  
Suppressive Therapy ◽  
Free Calcium ◽  
Carbonyl Cyanide ◽  
Intracellular Ca ◽  
Human Polymorphonuclear Leukocytes

Intracellular free calcium concentrations ([Ca++]1) were studied in polymorphonuclear leukocytes (PMNs) from 13 athyreotic patients who had been previously treated by total thyroidectomy and radioiodine therapy for differentiated thyroid carcinoma, and from age- and sex-matched euthyroid healthy controls. Patients were studied twice, when hypothyroid (visit 1) and after restoration of euthyroidism by L-T4 TSH-suppressive therapy (visit 2). PMNs from patients at visit 1 had significantly lower resting [Ca++]1 levels compared to both visit 2 and controls. Values at visit 2 did not differ from those of the controls. Stimulus-induced [Ca++]1 rise was also significantly blunted at visit 1 and normalized at visit 2, possibly through a differential contribution of distinct intracellular Ca++ stores, as suggested by the response pattern to the chemotactic agent, N-formyl-Met-Leu-Phe (fMLP), to the selective SERCA pump inhibitor, thapsigargine, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP). In vitro treatment of PMNs from healthy subjects with high TSH concentrations impaired intracellular Ca++ store function. Both resting [Ca++]1 levels and fMLP-induced [Ca++]1 rise increased in the presence either of low-concentration TSH or of T4, but effects of TSH and T4 were not additive. T3, rT3, and TRIAC had no effect. In conclusion, this study provides evidence for a direct relationship between thyroid status and [Ca[Ca++]1 homeostasis in human PMNs, mainly related to direct actions of TSH and T4 on these cells.

Chlorobutanol, a Preservative of Desmopressin, Inhibits Human Platelet Aggregation and Release In Vitro

1990 ◽  
Vol 64 (03) ◽  
pp. 473-477 ◽  
Author(s):  
Shih-Luen Chen ◽  
Wu-Chang Yang ◽  
Tung-Po Huang ◽  
Shiang Wann ◽  
Che-ming Teng
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Atp Release ◽  
Free Calcium ◽  
Dependent Manner ◽  
Antiplatelet Effect ◽  
Human Platelet Aggregation ◽  
Acid Pathway ◽  
Arachidonic Acid Pathway

SummaryTherapeutic preparations of desmopressin for parenteral use contain the preservative chlorobutanol (5 mg/ml). We show here that chlorobutanol is a potent inhibitor of platelet aggregation and release. It exhibited a significant inhibitory activity toward several aggregation inducers in a concentration- and time-dependent manner. Thromboxane B2 formation, ATP release, and elevation of cytosolic free calcium caused by collagen, ADP, epinephrine, arachidonic acid and thrombin respectively were markedly inhibited by chlorobutanol. Chlorobutanol had no effect on elastase- treated platelets and its antiplatelet effect could be reversed. It is concluded that the antiplatelet effect of chlorobutanol is mainly due to its inhibition on the arachidonic acid pathway but it is unlikely to have a nonspecitic toxic effect. This antiplatelet effect of chlorobutanol suggests that desmopressin, when administered for improving hemostasis, should not contain chlorobutanol as a preservative.

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