Protection of chronic intermittent hypobaric hypoxia against collagen-induced arthritis in rat through increasing apoptosis

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Author:
SHI Min(Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China;Department of Clinical Laboratory,Second Hospital,Hebei Medical University, Shijiazhuang 050017,China)
CUI Fang(Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China)
LIU Ai-Jing(Department of Immune and Rheumatism,Second Hospital, Hebei Medical University, Shijiazhuang 050017,China)
LI Jiao(Department of Clinical Laboratory,Second Hospital,Hebei Medical University, Shijiazhuang 050017,China)
MA Hui-Juan(Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China)
CHENG Ming(Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China)
YANG Jing(Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China)
ZHANG Yi(Department of Physiology, Hebei Medical University, Shijiazhuang 050017,China)
Journal Title:
ACTA PHYSIOLOGICA SINICA
Issue:
Volume 63, Issue 02, 2011
DOI:
Key Word:
collagen-induced arthritis;chronic intermittent hypobaric hypoxia;cell apoptosis;T lymphocytes;rat

Abstract: The aim of present study was to investigate the effect of chronic intermittent hypobaric hypoxia (CIHH) on collagen-induced arthritis (CIA) in rat. Fifty male adult Sprague-Dawley rats were randomly divided into 5 groups: CIHH pre-treatment group (Pre-T), pre-control group (Pre-C), CIHH post-treatment group (Post-T), post-control group (Post-C) and blank control group (Con).The rats in Pre-T and Post-T groups were exposed to 28 d of hypobaric hypoxia (simulated 3 000 m altitude, 5 h per day, pO2 = 108.8mmHg, 14% O2) in a hypobaric chamber before and 12 days after CIA induction, respectively. The rats in Pre-C and Post-C groups were only experienced CIA induction, being control groups for Pre-T and Post-T groups, respectively. The rats in Con group were not given any treatment. The thickness of two-hind paw of rat was measured with spiral micrometer and the degree of arthritis was evalu-ated by arthritis index (AI). Morphological changes of ankle joint were observed through HE staining. The apoptotic rate in synovial tissue was measured by terminal dUTP nick end labeling (TUNEL) and the apoptotic rate of CD3+ T lymphocyte in spleen was mea-sured by flow cytometry technique. The protein expressions of Bcl-2 and Bax were measured using immunohistochemistry SP meth-od. The results showed that incidence rate of CIA in Pre-T rats was lower than that in Pre-C rats (P<0.05). AI in Pre-T and Post-T rats were smaller than those in Pre-C and Post-C, respectively (P<0.05). In Pre-C and Post-C rats, there were hyperplasia of synovial cell, pannus forming, infiltration with inflammatory cell, and destroyed cartilage and bone in ankle joint. On the contrary, pathological changes of ankle joint were alleviated significantly in Pre-T and Post-T rats. Compared with Pre-C and Post-C rats, apoptotic rates of synovial cell and T lymphocyte in Pre-T and Post-T rats were increased (P<0.05). As to the possible anti-apoptosis mechanism,CIHH, no matter before and after CIA induction, decreased Bcl-2 expression and increased Bax expression in joint synovial cells and spleen T lymphocytes (P<0.05), respectively. In conclusion, CIHH possesses a protective effect against CIA in rat by enhancing apoptosis of synovial cells and T lymphocytes, which may be related to the inhibition of Bcl-2 protein expression and the promotion of Bax protein expression.

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