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BACKGROUND AND AIMS: Subarachnoid hemorrhage has complex, multisystem and multifaceted pathogenesis that involves several ongoing pathological processes, including BBB degradation. Our aim was to survey potential protective properties of minocycline on Tight Junctions (TJ) proteins in rat brain, after experimentally induced pre-chiasmatic SAH (pSAH). METHODS: pSAH was induced by injection of 200 μL of fresh autologous arterial blood into pre-chiasmatic cistern in rat brain. Minocycline was administrated ip twice, at 1st and 10th h after surgery (dose: 30 mg/kg). 24 h following the surgery, animals were perfused transcardialy and whole brains were collected. In order to investigate immuno-localization of TJ proteins, coronal sections were immuno-stained against Zonulin-1, Occludin and Claudin-5. ZO-1, OCN, CLN-5 proteins levels were examined by WB reactions. RESULTS: We observed numerous blood vessels around the site of blood application as well in more distant areas, where we found essential alterations in immunostaining patterns of ZO-1, OCN and CLN-5, comparing to controls. Minocycline administration preserves physiological ZO-1 and OCN cellular localization comparing to SAH group. Subsequently we provided WB reactions to define SAH impact on TJ protein level. We observed that SAH leads to significant decrease in both OCN and ZO-1 protein level in first 24 h after ictus. Important message comes from the minocycline experiment. We found out significant increase of ZO-1 level comparing to SAH group. Though OCN doesn’t reach significance, we can observe some positive trend in minocycline group. CONCLUSIONS: Administration of arterial blood directly to prechiasmatic cistern leads to serious affections of TJ integrity during first 24 h after pSAH. Minocycline protects TJ proteins from degradation and also preserves TJ unit from morphological alterations at the level of brain vessel endothelium.