Matrix metalloproteinase 2 activity decreases in human periodontal ligament fibroblast cultures submitted to simulated orthodontic force.

Orthodontic force compresses the periodontal ligament promoting the expression of pro-inflammatory mediators and matrix metalloproteinases responsible for tooth movement. The extent in time while periodontal cells are being treated and the increment in the amount of mechanical stress caused by the orthodontic force is thought to regulate the levels of metalloproteinases in the periodontal tissue. To study the possible regulation in the activity of metalloproteinases 2, 3, 7, 9, and 10 by simulated orthodontic force, human periodontal ligament fibroblast cultures were centrifuged (141 × g) for 30, 60, 90, and 120 min, simulating the orthodontic force. Cell viability, protein quantification, and activity of metalloproteinases by zymography were evaluated at 24, 48, and 72 h after centrifugation in both cell lysates and growth medium. The activity of the 72-kDa matrix metalloproteinase 2 was decreased at 24 h regardless of the duration of centrifugation and at 48 h in cells centrifuged for 30 min only. Decrease in the amount of total protein in lysates was seen at 48 and 72 h with no change in cell viability. The data seem to indicate that the amount of mechanical stress regulates the levels of secreted matrix metalloproteinase 2. In addition, the centrifugation as a model for simulated orthodontic force may be used as a simple and reliable method to study the role played by matrix metalloproteinases in periodontal ligament when submitted to mechanical force as occurring during tooth movement.

Scorpion venom increases mRNA expression of lung cytokines.

Previous studies have demonstrated that scorpion toxins increase the serum levels of IL-1, IL-6, INF-gamma, and GM-CSF in patients with severe shock and pulmonary edema. Moreover, it has been shown that experimental models of scorpion envenomation presented an increase in serum levels of IL-1, IL-6, IFN-gamma and nitric oxide. Thus, it is possible that the cytokine release may contribute to the onset and maintenance of the pulmonary edema induced by scorpion venom. This study was designed to investigate whether inflammatory and non-inflammatory cytokines, contribute to the pulmonary injury induced by infusion of Tityus serrulatus scorpion toxin in rats. We show that scorpion venom not only increases the expression of mRNA pulmonary inflammatory cytokines but also non-inflammatory cytokines as well. Moreover, the expression of IL-1alpha, IL-1beta and IL-6 mRNA was shown to be higher among the remaining detectable cytokines. The findings of this study provide additional insight towards the understanding of the pathophysiology of the pulmonary edema induced by scorpion venom. The increased level of pulmonary cytokines observed during the pulmonary edema may be responsible for the exacerbation and maintenance of the inflammatory response to scorpion venom in the lungs.

Effect of acid secretion blockade on acute gastric mucosal lesions induced by Tityus serrulatus scorpion toxin in anaesthetized rats.

Scorpion venom (TX) promotes gastric acid and pepsin secretion leading to acute gastric mucosal lesions (AGML), when injected in animals. The goal of the present study was to observe the effects of acid gastric secretion blockers over the incidence of TX-induced AGML in vivo. To verify this model, we used male albino rats, fasted 18-20 h (n=122) and anaesthetized with urethane (1.4 g/kg, i.p.). Their trachea and left femoral vein were both cannulated; the first to avoid airway obstructions during scorpion intoxication and the second for administration of saline, TX and acid blockers. Following the surgical procedure, the animals were divided in 10 groups of at least 10 animals each. Control groups were injected with NaCl 0.9% 1 ml/kg (n=10) or TX 375 microg/kg (n=32). Test groups (n=10, each) received atropine 5 mg/kg, cimetidine 10mg/kg, ranitidine 2.5mg/kg, ranitidine 5mg/kg, omeprazol 1 mg/kg, omeprazol 4 mg/kg, octreotide 80 and octreotide 100 microg/kg 10 min before the TX was injected. After 1h of intoxication, the stomach was resected for macroscopic study and the gastric secretion was collected for volume, pH and acid output assessment. We observed that all blockers were able to completely or partially prevent the TX-induced acid secretion as well as the AGML (p<0.05). Our data suggest the TX-induced AGML can be prevented by different class of acid blockers injected before the intoxication.

Systemic inflammatory response secondary to abdominal compartment syndrome: stage for multiple organ failure.

BACKGROUND: The abdominal compartment syndrome (ACS) has been implicated in the pathogenesis of postinjury multiple organ failure. The ACS is defined as intra-abdominal hypertension causing adverse physiologic response. This study was designed to determine the effects of IAH on the production of interleukin-1b (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha), and the effects on remote organ injury. METHODS: IAH was induced in Sprague-Dawley rats which were divided into 5 groups, 10 animals each. Intra-abdominal pressure (IAP) was increased to 20 mm Hg for 60 and 90 minutes in two different groups. In a third group following IAP of 20 mm Hg the abdomen was decompressed for 30 minutes before samples were collected. The other animals were used as controls. Hemodynamic response was monitored throughout the procedure. Cytokine levels were assessed in the plasma. Remote organ injury was assessed by histopathology and myeloperoxidase activity. RESULTS: IAH caused a significant decrease in MAP. After abdominal decompression MAP returned to baseline levels. A significant decrease in arterial pH was also noted. Increase in the levels of TNF-alpha and IL-6 was noted 30 minutes after abdominal decompression. Plasma concentration of IL-1b was elevated after 60 minutes of IAH. Abdominal decompression, however, did not cause a significant increase in the levels of this cytokine. Lung neutrophil accumulation was significantly elevated only after abdominal decompression. Histopathological findings showed intense pulmonary inflammatory infiltration including atelectasis and alveolar edema. CONCLUSIONS: IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF.