OBJECTIVETo investigate the effects of Qili Qiangxin capsules on the amino-terminal pro-brain natriuretic peptide (NT-proBNP) level and cardiac function in patients with silicosis.

METHODSHospitalized silicosis patients with heart failure were divided into treatment group (41 cases) and control group (30 cases) according to their own will. Both groups received comprehensive symptomatic treatment; in addition, the treatment group received Qili Qiangxin capsules. The treatment lasted 6 months. The observed items included NT-proBNP level, 6-minute walk test, ultrasonic cardiogram, and NYHA classification before and after treatment.

RESULTSAccording to NYHA classification, the response rate was 29.27%in the treatment group and 10.00%in the control group; there was a significant difference between the two groups (P < 0.05). The average walk distance in the treatment group was increased from 150.96±73.12 m before treatment to 169.32±77.04 m after treatment, and the improvement was statistically significant (P < 0.05). The average NT-proBNP level in the treatment group was reduced from 1154.44 ± 480.79 ng/L before treatment to 494.49 ± 342.61 ng/L after treatment, and the reduction was statistically significant (P < 0.01). Left ventricular ejection fraction was significantly improved in the treatment group (P < 0.05).

CONCLUSIONQili Qiangxin capsules in addition to comprehensive symptomatic treatment can significantly reduce NT-proBNP level and improve cardiac function in silicosis patients, and thereby improve patients' quality of life.

Capsules ; Drugs, Chinese Herbal ; pharmacology ; Echocardiography ; Heart Failure ; physiopathology ; Humans ; Natriuretic Peptide, Brain ; drug effects ; metabolism ; Peptide Fragments ; drug effects ; metabolism ; Quality of Life ; Silicosis ; drug therapy ; physiopathology

OBJECTIVE: To explore the protective effect of SBi4211 (heptamidine), an inhibitor of S100B, against central nervous system injury induced by HIV-1 envelope protein gp120. METHODS: In an RESULTS: In the cell co-culture system, SBi4211 treatment significantly inhibited gp120-induced expression of S100B, RAGE and GFAP in U251 cells ( CONCLUSIONS SBi4211 can protect neurons from gp120-induced neurotoxicity possibly by inhibiting the S100B/ RAGE-mediated signaling pathway.
Animals ; Astrocytes ; Blotting, Western ; Central Nervous System ; HIV Envelope Protein gp120 ; Mice ; Neurons ; S100 Calcium Binding Protein beta Subunit ; Signal Transduction