Protective mechanism of tetramethylpyrazine on cardiovascular system / 中国中药杂志

Tetramethylpyrazine is the main component of Ligusticum chuanxiong. Studies have found that tetramethylpyrazine has a good protective effect against cardiovascular diseases. In the heart, tetramethylpyrazine can reduce myocardial ischemia/reperfusion injury by inhibiting oxidative stress, regulating autophagy, and inhibiting cardiomyocyte apoptosis. Tetramethylpyrazine can also reduce the damage of cardiomyocytes caused by inflammation, relieve the fibrosis and hypertrophy of cardiomyocytes in infarcted myocardium, and inhibit the expansion of the cardiac cavity after myocardial infarction. In addition, tetramethylpyrazine also has a protective effect on the improvement of familial dilated cardiomyopathy. Besides, the mechanisms of tetramethylpyrazine on blood vessels are more abundant. It can inhibit endothelial cell apoptosis by reducing oxidative stress, maintain vascular endothelial function and homeostasis by inhibiting inflammation and glycocalyx degradation, and protect vascular endothelial cells by reducing iron overload. Tetramethylpyrazine also has a certain inhibitory effect on thrombosis. It can play an anti-thrombotic effect by reducing inflammatory factors and adhesion molecules, inhibiting platelet aggregation, and suppressing the expression of fibrinogen and von Willebrand factor. In addition, tetramethylpyrazine can also reduce the level of blood lipid in apolipoprotein E-deficient mice, inhibit the subcutaneous deposition of lipids, inhibit the transformation of macrophages into foam cells, and inhibit the proliferation and migration of vascular smooth muscle cells, thereby reducing the formation of atherosclerotic plaque. In combination with network pharmacology, the protective mechanism of tetramethylpyrazine on the cardiovascular system may be mainly achieved through the regulation of phosphatidylinositol 3 kinase/protein kinase B(PI3K/Akt), hypoxia-inducible factor 1(HIF-1), and mitogen-activated protein kinase(MAPK) pathways. Tetramethylpyrazine hydrochloride and sodium chloride injection has been approved for clinical application, but some adverse reactions have been found in clinical application, which need to be paid attention to.

NADPH oxidase inhibitor apocynin attenuates ischemia/reperfusion induced myocardial injury in rats / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the role of NADPH oxidase inhibitor apocynin on ischemia/reperfusion (I/R)-induced myocardial injury.</p><p><b>METHODS</b>Male SD rat hearts were divided into the normal control group; sham group; I/R group (1 h ischemia followed by 3 h reperfusion); I/R + apocynin group (50 mg/kg, administrated at 30 min before reperfusion) and I/R + vehicle group (same volume vehicle administrated at 30 min before reperfusion). At the end of reperfusion, myocardial infarct size, apoptosis, plasma CK activity, myocardial NOX activity, myocardial caspase-3 expression and activity, myocardial mRNA and protein expressions of vascular peroxidase 1 (VPO1) and NOX2 were measured.</p><p><b>RESULTS</b>Infarct size, ratio of cardiomyocyte apoptosis, mRNA and protein expression of VOP1 and NOX2, serum CK, myocardial NOX and caspase-3 activities in the I/R group were all significantly increased compared to those in the sham group (P < 0.01). Above parameters were similar between I/R + vehicle group and I/R group (all P > 0.05). Infarct size, ratio of cardiomyocyte apoptosis, myocardial mRNA and protein expression of VOP1 and NOX2, serum CK, myocardial NOX and caspase-3 activities were significantly lower in I/R + apocynin group compared to those in I/R group (all P < 0.01).</p><p><b>CONCLUSIONS</b>NOX/VPO pathway plays an important role in mediating I/R-induced myocardial oxidative injury. NOX inhibition could reduce I/R-induced myocardial oxidative injury by attenuating myocardial apoptosis in this model.</p>

Effects of oxymetazoline hydrochloride on ex vivo human nasal cilia movement measured with high-speed digital microscopy / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the effects of oxymetazoline hydrochloride on ex vivo human nasal cilia movement.</p><p><b>METHODS</b>Ciliary beat frequency (CBF) of cultured human nasal epithelial cells was measured by high-speed digital microscopy in HBSS and oxymetazoline hydrochloride of different concentrations in 20 minutes. RESULTS; CBF of cultured nasal epithelial cells in HBSS and 0.25 g/L oxymetazoline hydrochloride did not show significant changes in 20 minutes (F = 0.098, P = 1.00). However, in 0.50 g/L and 1.00 g/L oxymetazoline hydrochloride, CBF increased slightly in 3 -4 minutes and reached the apex, then decreased gradually. At the end of observation, CBF showed no significant difference in 0.50 g/L, (F = 2.94, P = 0.05) but there was a significant lower CBF in 1.00 g/L. In the first 3 minutes, the CBF in 2.00 g/L oxymetazoline hydrochloride was stable, and then slowed gradually. After 16 minutes, there was significant difference. In initial, the highest normalized CBF of each group showed no significant difference. However, the lowest normalized CBF of 1.00 and 2.00 g/L oxymetazoline hydrochloride showed a significant difference with HBSS, 0.25 and 0.50 g/L oxymetazoline hydrochloride.</p><p><b>CONCLUSIONS</b>Oxymetazoline had a concentration-dependent inhibitory effect on cultured human nasal CBF from 0.25 to 2.00 g/L. The inhibitory effect increased with the concentration going up. Oxymetazoline hydrochloride of 0.50 g/L might be the optimal choice for clinical application.</p>

Anatomical and computed tomographic analysis of the interaction between uncinate process and agger nasi cells / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the anatomical interaction between uncinate process and agger nasi cell to better understand the anatomy of the frontal sinus drainage pathway by endoscopy, spiral computed tomography (CT) and sectioning.</p><p><b>METHODS</b>Twenty-one skeletal skulls (forty-two sides) and one cadaver head (two sides) were studied by spiral CT together with endoscopy and collodion embedded thin sectioning at coronal plane. The sections with the thickness of 100 microm were stained with hemotoxylin and eosin.</p><p><b>RESULTS</b>Under endoscopy, a leaflet of bone to the middle turbinate, which is given off by uncinate process, forms the anterior insertion of the middle turbinate onto the lateral nasal wall. The middle portion of the uncinate process attached to the frontal process of the maxilla in all of the skeletal nasal cavities, as well as the lacrimal bone in 78.6% of the skeletal nasal cavities. On CT scans, the agger nasi cell is present in 90.5% of the skeletal nasal cavities. While the lateral wall of the agger nasi cell is formed by lacrimal bone, the medial wall of the agger nasi cell is formed by uncinate process. And the anterior wall is formed by the frontal process of the maxilla. The superior portion of the uncinate process forms the medial, posterior and top wall of the agger nasi cells. The superior portion of the uncinate extends into the frontal recess and may insert into lamina papyracea (33.3%), skull base (9.5%), middle turbinate, combination of these (57.2%).</p><p><b>CONCLUSIONS</b>The agger nasi cell is the key that unlocks the frontal recess.</p>