<p class="first" id="d8118836e101">Inflammatory response caused by early weaning stress
in piglets is associated with
various diseases. The Hippophae rhamnoides polysaccharide (HRP) exhibits anti-inflammatory
activity and immunomodulatory properties. The mechanisms for the protective effects
of HRP on barrier function, inflammatory damage and apoptosis in intestinal porcine
epithelial cells (IPEC-J2) induced by the lipopolysaccharide (LPS) are unknown. In
this study, we first demonstrated the cytotoxicity of HRP-induced IPEC-J2 cells by
reducing cell viability. IPEC-J2 cells were treated with 0-800 μg/mL doses of HRP,
and 0-600 μg/mL doses were used in further experiments. Upon exposure to LPS, the
viability of IPEC-J2 cells, ROS production, immunoglobulin levels (immunoglobulin
M (IgM), immunoglobulin A (IgA) and immunoglobulin G (IgG)) and tight junction protein
level (zonula occludens-1 (ZO-1), occluding, claudin-1) decreased. Inflammatory factors
(interleukin-1beta (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis
factor-alpha (TNF-α)) and apoptosis (Bcl-2, Bax, caspase-3, caspase-8 and caspase-9)
were increased. Cell morphology and internal structure were damaged in the LPS treatment.
Pre-treating cells with HRP (0-600 μg/mL) reduced inflammatory factors levels, apoptosis
rate, increased immunoglobulins, tight junction protein levels and relieved cell surface
morphology damage. Pre-treatment with HRP also reduced the levels of the Toll-like
receptor 4 (TLR4) and Myeloid differentiation factor 88 (MyD88) and inhibited the
phosphorylated NF-κB factor-kappa B (NF-κB) in cells induced by LPS. These results
show that pre-treatment with HRP protected against LPS-induced IPEC-J2 cell damage
through its anti-inflammatory activity.
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