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Bajaj S., Garrido C., Hirschfeld F., Hakimiyan A., Rappoport L., Oegema T.

Animal Study with a reported sample of 17 on Osteoarthritis, Cartilage Damage, Ankle Injury, Chronic Inflammation, published in Cartilage (2009) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Cartilage (2009)
Reported sample size
17
Source database
Europe PMC
PMCID
PMC4513501

Abstract (original English)

Introduction Objectives: To investigate the effect and understand the mechanism of action of P188 surfactant on cartilage degeneration and cell survival in acute trauma to human ankle cartilage. Methods and Materials Sixteen normal tali were impacted using a 4mm indenter with 600N. 8mm cartilage plugs containing the 4mm impacted core and 4mm immediately adjacent non-impacted ring were removed and cultured with or without P188. Results were assessed by layers at 0,2,7 and 14 days after injury with live/dead, Tunel assays and histology with Safranin-O/fast green staining. P188 mode of action was assessed via its regulations of IL-6 and MAPK signaling using Western blots. Results A single impact to human articular cartilage resulted in cell death at the impaction site and radial progression of apoptosis to adjacent ring. P188 promoted cell survival by reducing cell death more than 2-fold (p⇠0.05) in the core and about 30% in the ring as compared to all untreated controls. It also inhibited expansion of apoptosis in the ring especially within first 7 days post impaction (7.5% Tunel-positive cells vs 46% in the untreated control; p⇠0.01). In the current study P188 mediated its effect through the inhibition of phosphorylation of MAPK/ERK JNK, and p38 and attenuation of IL-6 signaling via inhibition of Stat1 and Stat3; furthermore, phosphorylation of ATF2 (downstream in P38 pathway) w

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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