Neuronal immunoreactivity for mannose-binding lectin after venous occlusion-induced focal cerebral ischemia in rats

A recent research reveals that complement activation exacerbates cerebral infarction. However, involvement of the lectin pathway, (the third complement activation pathway) in cerebral ischemia is not well studied. In this study, we investigated the appearance of mannose-binding lectin (MBL) in ischemic brain tissue. Male Wistar rats (n = 25) were divided into three groups: untreated control, sham, and vein occlusion (VO). Rats in the VO group had two adjacent photochemically occluded cortical veins. Regional cerebral blood flow (rCBF) was measured in the sham and VO groups. Rats were perfusion-fixed at 72 h in the sham group and at 3, 24, and 72 h after inducing ischemia in the VO group. Neuronal immunoreactivity for MBL, C1q, C3, and C5b-9 was graded on a scale from 0 (no staining) to 4 (strong immunoreactivity). rCBF significantly decreased in the VO group compared to the sham group. Immunohistochemical staining results were negative in the control group. MBL immunoreactivity was significant increased at 24 and 72 h after inducing ischemia in the VO group compared to the sham group. After inducing ischemia, C1 immunoreactivity was significantly increased at 3, 24, and 72 h, while C3 immunoreactivity increased at 72 h. C5b-9 immunoreactivity exhibited a tendency for only positive staining. In brain tissue after focal cerebral ischemia, MBL expression, as well as C1q and C3, appeared at 3 h, peaked at 24 h, and was maintained at 72 h. These results suggest that an MBL inhibitor administered during the relatively early ischemic phase might attenuate tissue damage.