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ANALISI DELLA MORTE CELLULARE INDOTTA DAL CISPLATINO E STUDIO DI EVENTUALI SOSTANZE PROTETTIVE SU MODELLI IN VITRO
No full textCisplatin (cis-DDP) is a chemotherapy agent that is used as a
treatment for several types of cancer. Unfortunately it could injure several
areas of the cochlea, including outer hair cells in the Organ of Corti, the spiral ganglion and the stria vascularis. Cis-DDP has been shown to
induce auditory sensory cell apoptosis in vitro and in vivo. The
mechanisms appear to involve the production of reactive oxygen species
(ROS) and depletion of antioxidant enzymes which can trigger cell death.
Approaches to chemoprevention include the administration of
antioxidants to protect against ROS. The Ginkgo biloba extract (EGb 761 o
Ginkgoselect®) is known to have antioxidant proprieties with a free
radicals scavenging effect, and protecting cells against apoptosis. It has
been used for otoprotection study only in vivo model, with positive effects.
One of the goal of this study was that to verify the protective effects of
ginkgoselect on a mouse inner ear cell line (OC-k3). Our data showed that
Ginkgo biloba extract protects against cisplatin-induced ototoxicity.
The calcium ion (Ca2+) regulates hair and neuronal cells function in
the inner ear. It’s involved in the mechanical signal transduction, and
release of neurotransmitters. Changes in its intracellular concentration
determines the cell’s fate. It’s a second messenger that regulates the
activation of proteins involved in apoptosis. Calcium channel antagonist
drugs was studied as another mechanism to protect cells from cisplatin
ototoxicity. Flunarizine is a calcium blocker drug, currently used to treat
diseases of the inner ear, such as vertigo. There are very few data on
flunarizine protective effect against cisplatin damages. The PC12 cell (rat
pheochromocytoma cell line) within several days of NGF exposure,
differentiate in sym-pathetic neurons, it’s therefore always used as a
neuronal model. In this thesis we have been evaluated the cisplatin toxicity
on these cells, undifferentiated and differentiated, and the ability of
flunarizina to protect cells, in order to conduct a basic survey focused on
the mechanism of both drugs. In sum, flunarizina is a good protector
against the cisplatin toxicity, it’s able to preventing apoptosis by acting on
expression of proteins involved in programmed cell death (14-3-3β, protein kinase C and GAPDH). Present results are of great interest to conduct
further investigations on spiral ganglion primary neurons cultures.
Key words: inner ear, OC-k3, PC12, cisplatin, Ginkgo biloba,
flunarizine, apoptosis
Phagocytosis of pancears rodlet cells by immune cells of infected Phoxinus phoxinus. In: 17thInternational conference of the World Association for the Advancement of Veterinary Parasitology.
No full textParasite load, life cycle and histopathology of Leptorhynchoides plagicephalus (Acanthocephala) from Acipenser naccarii in the River Po.
No full textOC-k3 cells, an in vitro model for cochlear implant biocompatibility
No full textObjective: In patients with severe or deep hypoacousis, the cochlear implant represents the only way to recover the ability to hear. Nevertheless, the insertion of a silicone-embedded electrode in the cochlea may produce damage through pressure, shock, bleeding and tissue perforation, which could cause apoptosis and necrosis in the organ of Corti. Another variable is the use of different silicone materials. Although all embedding silicone compounds are medical grade biocompatible, their effects in the inner ear environment have never been tested. Our aim was to assess whether polydimethylsiloxane (PDMS) compounds employed in cochlear implants could be cytotoxic to inner ear cells, by exposing an in vitro organ of Corti cell line (OC-k3) to four PMDS compounds (three fluid and one elastomere) and verifying whether or not any one of these compounds could lead to cell death by apoptosis or necrosis. Study design: To obtain a toxicity curve, OC-k3 cells were exposed to PDMS compounds (octadimethylsiloxane, hexadimethylsiloxane, decamethylcyclopentasiloxane and a silicon rod) at different dilutions and time of exposure, testing vitality by flux cytofluorometry and fluorescence microscopy. Investigations were extended to molecular interactions between OC-k3 cells and PDMS, testing cell death markers by immunocytochemistry and real-Time PCR. Results: Among the fluid PDMS compounds, decamethylcyclopentasiloxane induced the highest significant cell mortality (at 1:100 dilution) after 48 h of treatment, followed by octadimethylsiloxane (1:10) and hexadimethylsiloxane (1:5) at 24 h. The silicon rod did not show any inner ear cell toxicity. Conclusion: In our experimental conditions, the observed cell mortality was not caused by release of cytotoxic molecules by PDMS on OC-k3 cells, but by the formation by PMDS of a surface film preventing air exchange. From a biomolecular point of view, PDMS compounds appear suitable for electrode coating in cochlear implants. © 2015 International Association of Physicians in Audiology
Alterations in the neuroendocrine system of swimbladder of the European eel infected with Anguillicola crassus (Nematoda: Dracunculoidea).
No full textIn vitro protective effects of Ginkgo biloba against cisplatin toxicity in mouse cell line OCk3
No full textCisplatin is one of the most common agents employed in standard treatments of a variety of malignant tumours. However, its clinical application is limited because of serious and sometimes irreversible side-effects, which include ototoxicity. As a result of cisplatin treatment, several areas of the cochlea are damaged, including outer hair cells in the organ of Corti, spiral ganglion and the stria vascularis. Notwithstanding extensive research, the available treatments to prevent ototoxicity are not very effective. Cisplatin is thought to interfere with the production of endogenous antioxidants that protect the inner ear against reactive oxygen species (ROS). Outer hair cells are the most sensitive to ROS damage, which can lead to apoptosis. Strategies of chemoprevention include the administration of antioxidants to protect hair cells at an early stage in the ototoxic pathways. In this study we evaluated the protective effects of a nutraceutical product compound with antioxidant activity (ACUVAL®, Scharper Healthcare, Italy). Ginkgo biloba is known for having antioxidant properties and for this reason we used cytofluorimetry to test the otoprotective effects of Ginkgo biloba extract (Ginkgoselect® Phytosome®, Indena) against cisplatin induced toxicity in a mouse inner ear cell line (OCk3). The results support the hypothesis that pre-treatment with Ginkgo biloba extract (50-150 μg/ml) is able to protect OCk3 against cisplatin induced toxicity
Polydimethylsiloxanes biocompatibility in PC12 neuronal cell line
No full textCochlear implants, the only way to recover from severe/profound hearing loss, may cause adverse effects, among which reactions to silicone materials coating implant electrodes, leading to apoptosis and necrosis of spiral ganglion cells. Our aim was to evaluate whether three polydimethylsiloxane (PDMS) compounds (hexadimethylsiloxane, octamethyltrisiloxane, decamethylcyclopentasiloxane) used in silicone rods could exert toxic effects on an in vitro neuronal cell model (PC12). Cell viability, morphology and mRNA expression levels of apoptotic markers were evaluated on PC12 cells at different PDMS dilutions up to 6 days of exposure. The results showed that at the highest concentrations tested cell viability was reduced by hexadimethylsiloxane and octamethyltrisiloxane at all times of exposure, but only from 72 h onwards by decamethylcyclopentasiloxane. The number of neurites per cell was not affected by hexadimethylsiloxane, but was significantly reduced from 24 h onwards by octamethyltrisiloxane and decamethylcyclopentasiloxane. Neurite length was reduced by hexadimethylsiloxane only at 24 h, and by octamethyltrisiloxane and decamethylcyclopentasiloxane at all exposure intervals. In controls exposed to silicone or glass rods cell viability was reduced only after 24 h, but neurite number and length was never reduced at any exposure interval. Biomolecular investigations showed that apoptotic markers did not change in any experimental condition, suggesting that PDMS are biocompatible. The reduction of cell viability and neurite number and length caused by exposure to these compounds was probably caused by a PDMS surface film formed over the cell medium, preventing air exchange, and not by the release of cytotoxic molecules
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