ABSTRACT
BACKGROUND:To inhibit the expressions of prothrombin activator inhibitor 1 and tissue plasminogen activator is one potential target for the treatment of cerebral infarction. OBJECTIVE:To investigate the expressions of serum inflammatory cytokines in rats with cerebral infarction undergoing bone marrow mesenchymal stem cel transplantation combined with edaravone. METHODS:Sixty Sprague-Dawley rats were enrol ed to prepare models of focal cerebral infarction by middle cerebral artery occlusion, and were randomly divided into four groups. Rats were given intravenous injection of PBS via tail veins for 5 consecutive days as model group, rats were subjected to intravenous injection of 2.0×109/L bone marrow mesenchymal stem cel suspension (1 mL) via tail veins, twice daily for 5 days as stem cel transplantation group, and those were given intravenous injection of 30 mg edaravone combined with intravenous injection of 2.0×109/L bone marrow mesenchymal stem cel suspension (1 mL) via tail veins for 5 days, twice daily, as combined group. RESULTS AND CONCLUSION:Compared with the model group, modified neurologic severity scores were lower, expressions of serum prothrombin activator inhibitor 1 and tumor necrosis factor-αmRNA in the brain decreased, and the infarct area reduced in the stem cel transplantation and combined groups. And the changed levels of above indicators in the combined group were significantly larger than those of the stem cel transplantation group. In conclusion, combination of bone marrow mesenchymal stem cel transplantation with edaravone can promote neural function recovery after cerebral infarction.
ABSTRACT
BACKGROUND:Studies have shown that human telomerase reverse transcriptase (hTERT) has the ability to enhance cel proliferation, maintain telomere length, prolonged cel life cultured in vitro. OBJECTIVE:To observe the effect of hTERT gene-modified bone marrow mesechymal stem cel transplantation on neural function recovery of rats with cerebral infarction. METHODS:Rat models of middle cerebral artery occlusion were established and randomized into model group, cel transplantation group and hTERT-modified cel transplantation group, with 20 rats in each group. Rats in the three groups were respectively injected via tail vein with 1 mL PBS, passage 9 bone marrow mesenchymal stem cel suspension (2.5×107/L) and hTERT-modified passage 9 bone marrow mesenchymal stem cel suspension (2.5×107/L), respectively. Modified neurological severity scores were determined before and after transplantation; RT-PCR and western blot assay were used to measure hTERT expression at gene and protein levels; TUNEL method was adopted to detect cel apoptosis in the brain. RESULTS AND CONCLUSION:hTERT-modified bone marrow mesenchymal stem cels had prolonged cel cycle, and with the increase in passage number, the cels showed good growth with no changes in morphology. The expressions of hTERT mRNA and protein were superior in the hTERT-modified cel transplantation group than the cel transplantation group, and there was a significant difference (P < 0.05). Modified neurological severity scores and number of apoptotic cels were decreased significantly in the hTERT-modified cel transplantation group compared with the other two groups (P < 0.05). These findings indicate that hTERT-modified bone marrow mesenchymal stem cels can promote neural functional recovery of rats with cerebral infarction.
ABSTRACT
BACKGROUND:Numerous clinical studies have confirmed that the microenvironment at a spinal cord injury site can be obviously improved through hyperbaric oxygen therapy; however, what effect does hyperbaric oxygen have on the microenvironment of the injured brain? OBJECTIVE:To investigate the effect of hyperbaric oxygen therapy on nerve regeneration microenvironment and the recovery of rat nerve function after focal cerebral infarction. METHODS:Rat models of focal cerebral infarction were established by occlusion of the middle cerebral artery and subjected to hyperbaric oxygen therapy. Sham group and model group were established as comparison. In the sham group, rat models of focal cerebral infarction were established but did not receive any treatment. Rats in the model group were placed in a hyperbaric oxygen therapy chamber but the pressure and oxygen concentration were not administered. RESULTS AND CONCLUSION:Compared with the model group, the score of rat limb function at 16 days after treatment and the expression of growth associated protein 43 in the rat cerebral infarcted area at postoperative 14 days were significantly increased , but infarct volume at postoperative 24 hours was al significantly decreased in the hyperbaric oxygen therapy group (alP < 0.05). These results confirmed that hyperbaric oxygen therapy can improve nerve regeneration microenvironment and promote the recovery of rat nerve function after focal cerebral infarction.