[Periodontitis Promotes the Progression of Oral Squamous Cell Carcinoma by Inducing Macrophage M2 Polarization].

Objective: To investigate the role of periodontitis in the development of oral squamous cell carcinoma (OSCC) and to determine whether periodontitis microorganisms induce M2 macrophage (M2) polarization and promote tumor progression.

Methods: The tumor tissues of OSCC patients with periodontitis and those without periodontitis were collected and immunohistochemistry tests were done to validate the trend of changes in M2 macrophages. A mouse model of OSCC accompanied by periodontitis was established by treating mice with drinking water containing four antibiotics for three consecutive days, applying in the mouths of the mice a coat of bacteria collected from the saliva of patients with periodontitis once every other day for five times, and injecting in their buccal mucosa OSCC cells (SCC7).

[Synergistic Antibacterial Activity of Berberine in Combination with Amylmetacresol Against ].

Objective: To study the antibacterial effect of berberine combined with amylmetacresol on .

Methods: Both dilution method and live bacteria CFU were used to determine the minimum inhibitory concentration (MIC) of berberine and amylmetacresol on . The killing effect of berberine and amylmetacresol on planktonic was detected by suspension quantitative germicidal test and live/dead bacteria staining.

[Mechanisms of cardioprotection induced by preconditioning after activation of MITOK(ATP) channel].

Aim: To determine mechanisms of cardioprotection induced by combination angiotensin-converting enzyme inhibitors (ACEI) with subthreshold preconditioning after activation of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel.

Methods: The Langendorff model of isolated rat heart was used. The time of the onset of uncoupling, the activities of sarcolemmal Na+/K+ -ATPase and Ca2+/Mg2+ -ATPase were measured.

[Angiotensin-converting enzyme inhibitors potentiate subthreshold preconditioning through NO and mitoK(ATP) channel.].

The aim of the present study was to determine whether angiotensin-converting enzyme inhibitors (ACEI) could contribute to the protective effects of preconditioning, and to explore its underlying mechanism. The Langendorff model of isolated rat heart was used. Cardiac contractility and lactate dehydrogenase (LDH) in the coronary effluent were measured, and infarct area of hearts after 30 min of ischemia followed by 120 min of reperfusion was analyzed.