M AMIR SHARIFI

Rhumatologue

📍 PLAISIR (78)MixteRPPS 10001358349

✨ Profil synthétique

IA · 19/05/2026

Le Dr Amir Sharifi est un rhumatologue exerçant à Plaisir. Ses recherches portent principalement sur les maladies du foie et les infections gastroentestinales, avec un h-index de 10 et 18 publications. Ses travaux publiés sur PubMed couvrent diverses pathologies, notamment les tendinopathies et les thérapies anti-TNF.

Expertises présumées

Tendinopathies
Thérapies anti-TNF
Épidémiologie des maladies rhumatismales
Revue et méta-analyse en rhumatologie
Maladies du foie
Infections gastroentestinales
Hépatite B et C

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

✨ Génération du profil synthétique IA en cours…

Lieux de consultation(4)

CABINET DU DR AMIR SHARIFI
13 RUE PASTEUR, 78370 PLAISIR
☎ 0130553088Activité de soin et de pharmacie
CENTRE HOSPITALIER DE PLAISIR
220 R MANSART BP 19, 78375 PLAISIR CEDEX
☎ 0130795700Activité de soin et de pharmacie🏥 Centre CH ↗

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.

Top publications · les plus citées

Protective Effect of Ginger (Zingiber officinale Roscoe) Extract against Oxidative Stress and Mitochondrial Apoptosis Induced by Interleukin-1β in Cultured Chondrocytes

Cells, tissues, organs · 2017

📚 65 citations🎯 RCR 3.73Top 12% NIH

Lire l'abstract Crossref ↓

Aims: The protective effects of ginger (Zingiber officinale Roscoe) extract on IL-1β-mediated oxidative stress and mitochondrial apoptosis were investigated in C28I2 human chondrocytes. Methods: The effects of various concentrations of ginger extract on C28I2 human chondrocyte viability were evaluated in order to obtain noncytotoxic concentrations of the drug by methylthiotetrazole assay. The cells were pretreated with 5 and 25 μg/mL ginger extract for 24 h, followed by incubation with IL-1β (10 ng/mL) for 24 h. The effects of ginger extract on IL-1β-induced intracellular reactive oxygen species (ROS) production and lipid peroxidation were examined. The mRNA expressions of antioxidant enzymes including catalase, superoxide dismutase-1, glutathione peroxidase-1, glutathione peroxidase-3, and glutathione peroxidase-4 were evaluated by reverse transcription polymerase chain reaction. The protein expressions of Bax, Bcl-2, and caspase-3 were analyzed by Western blotting. Results: No cytotoxicity was observed at any concentration of ginger extract in C28I2 cells. Ginger extract pretreatment remarkably increased the gene expression of antioxidant enzymes and reduced the IL-1β-induced elevation of ROS, lipid peroxidation, the Bax/Bcl-2 ratio, and caspase-3 activity. Conclusions: Ginger extract could considerably reduce IL-1β-induced oxidative stress and consequent mitochondrial apoptosis as the major mechanisms of chondrocyte cell death. These beneficial effects of ginger extract may be due to its antioxidant properties. It may be considered as a natural herbal product to prevent OA-induced cartilage destruction in the clinical setting.

Role of Simvastatin on fracture healing and osteoporosis: a systematic review on in vivo investigations

Clinical and experimental pharmacology & physiology · 2016

📚 44 citations🎯 RCR 2.38Top 22% NIH

Lire l'abstract Crossref ↓

SummarySimvastatin is a lipid lowering drug whose beneficial role on bone metabolism was discovered in 1999. Severalin vivostudies evaluated its role on osteoporosis and fracture healing, however, controversial results are seen in the literature. For this reason, Simvastatin has not been the focus of any clinical trials as yet. This systematic review clears the mechanisms of action of Simvastatin on bone metabolism and focuses onin vivoinvestigations that have evaluated its role on osteoporosis and fracture repair to find out (i) whether Simvastatin is effective on treatment of osteoporosis and fracture repair, and (ii) which of the many available protocols may have the ability to be translated in the clinical setting. Simvastatin induces osteoinduction by increasing osteoblast activity and differentiation and inhibiting their apoptosis. It also reduces osteoclastogenesis by decreasing both the number and activity of osteoclasts and their differentiation. Controversial results between thein vivostudies are mostly due to the differences in the route of administration, dose, dosage and carrier type. Local delivery of Simvastatin through controlled drug delivery systems with much lower doses and dosages than the systemic route seems to be the most valuable option in fracture healing. However, systemic delivery of Simvastatin with much higher doses and dosages than the clinical ones seems to be effective in managing osteoporosis. Simvastatin, in a particular range of doses and dosages, may be beneficial in managing osteoporosis and fracture injuries. This review showed that Simvastatin is effective in the treatment of osteoporosis and fracture healing.

Evaluating the Protective Effects and Mechanisms of Diallyl Disulfide on Interlukin-1β-Induced Oxidative Stress and Mitochondrial Apoptotic Signaling Pathways in Cultured Chondrocytes

Journal of cellular biochemistry · 2017

📚 33 citations🎯 RCR 1.58

Lire l'abstract Crossref ↓

ABSTRACTThe protective effects and mechanisms of DADS on IL‐1β‐mediated oxidative stress and mitochondrial apoptosis were investigated in C28I2 human chondrocytes. The effect of various concentrations of DADS (1, 5 10, 25, 50, and 100 μM) on C28I2 cell viability was evaluated in different times (2, 4, 8, 16, and 24 h) to obtain the non‐cytotoxic concentrations of drug by MTT‐assay. The protective effect of non‐toxic concentrations of DADS on experimentally induced oxidative stress and apoptosis by IL‐1β in C28I2 was evaluated. The effects of DADS on IL‐1β‐induced intracellular ROS production and lipid peroxidation were detected and the proteins expression of Nrf2, Bax, Bcl‐2, caspase‐3, total and phosphorylated JNK, and P38 MAPKs were analyzed by Western blotting. The mRNA expression of detoxifying phase II/antioxidant enzymes including heme oxygenase‐1, NAD(P)H quinine oxidoreductase, glutathione S‐transferase‐P1, catalase, superoxide dismutase‐1, glutathione peroxidase‐1, ‐3, ‐4 were evaluated by reverse transcription‐polymerase chain reaction. DADS in 1, 5, 10, and 25 μM concentrations had no cytotoxic effect after 24 h. Pretreatment with DADS remarkably increased Nrf2 nuclear translocation as well as the genes expression of detoxifying phase II/antioxidant enzymes and reduced IL‐1β‐induced elevation of ROS, lipid peroxidation, Bax/Bcl‐2 ratio, caspase‐3 activation, and JNK and P38 phosphorylation. DADS could considerably reduce IL‐1β‐induced oxidative stress and consequent mitochondrial apoptosis, as the major mechanisms of chondrocyte cell death in an experimental model of osteoarthritis. It may be considered as natural product in protecting OA‐induced cartilage damage in clinical setting. J. Cell. Biochem. 118: 1879–1888, 2017. © 2017 Wiley Periodicals, Inc.

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Top publications · les plus citées

Publications scientifiques (35) — classées par pathologie

Transversal21

Revue générale4

Case report / série2

Épidémiologie & registres2

Revue / méta-analyse2

Tendinopathies & SCC2

Anti-TNF1

Essai clinique1

IA en rhumatologie1

Pharmacovigilance1

Sclérodermie1

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