Kallistatin alleviates heart failure in rats by inhibiting myocardial inflammation and apoptosis via regulating sirt1.

OBJECTIVE: Heart failure (HF) is the loss of myocardial structure and function caused by various congenital or acquired heart diseases. This study explored the new target of treatment of HF by investigating the effect of Kallistatin (KS) on inflammation and apoptosis of myocardial tissue in HF rats. MATERIALS AND METHODS: We used doxorubicin to induce rat HF, and determined the success rate of modeling by detecting changes in rat heart weight and body weight, cardiac function and histology. We used two different doses (1 mg/kg, 2 mg/kg) of KS intraperitoneally injected rats and detected changes in inflammation and apoptosis of rat myocardial tissue by enzyme-linked immunosorbent assay (ELISA), Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and immunohistochemical staining. Changes in the expression of sirt1 were also detected. In addition, we cultured rat myocardial cell line, H9c2 cells, and used siRNA-sirt1 to inhibit sirt1 in H9c2 cells to clarify the mechanism of KS regulating myocardial cells. RESULTS: The body weight of HF rats treated with KS decreased while the heart weight increased. KS has also been found to reduce the concentration of brain natriuretic polypeptide (BNP) in rat serum. The results of echocardiography showed that KS effectively relieved the cardiac function of HF rats. Inflammatory factors (interleukin (IL)-1ß, IL-6, IL-8 and tumor necrosis factor (TNF)-α) and pro-apoptotic molecules (caspase3/9 and Bax) in the serum and myocardial tissue of rats treated with KS were also significantly reduced. The inhibition of sirt1 in H9c2 cells significantly reduced the anti-apoptotic effect of KS on H9c2 cells. CONCLUSIONS: KS reduces the inflammation and apoptosis of myocardial tissue in HF rats by promoting the expression of sirt1, thereby alleviating HF-induced myocardial injury.

Efficacy of lumbar cistern drainage combined with intrathecal antibiotherapy for the treatment of ventriculo-subarachnoid infections following surgery for hypertensive intracerebral hemorrhage.

OBJECTIVE: The aim of this study was to investigate the efficacy of lumbar cistern drainage combined with intrathecal injection of antibiotics (LCD-ITI) in treating postoperative intracranial infections of hypertensive intracerebral hemorrhage (pHIH-ICI). METHODS: Sixty pHIH-ICI patients were randomly divided into the control group and the treatment group, with 30 patients in each group. Conventional treatment was performed in the control group, while LCD-ITI was performed in the treatment group. The clinical outcomes, Glasgow Outcome Score (GOS), activities of daily living (ADL) scores, incidence rates of hydrocephalus and other indicators were compared. RESULTS: The improvement time of clinical symptoms, infection control time and hydrocephalus incidence of the treatment group were significantly lower than the control group (P<0.05). Also the infection control rate, GOS score and ADL score of the treatment group were significantly higher or better than the control group (P<0.05). CONCLUSION: LCD-ITI could improve clinical treatment and prognosis of pHIH-ICI patients.

Identification and characterization of a 30K glycoprotein of herpes simplex virus type 2.

A herpes simplex virus type 2 (HSV-2) type-specific monoclonal antibody (MAb), CH-A9, precipitated a glycoprotein with an M(r) of approximately 30,000 (g30K) from extracts of HSV-2-infected BHK cells labelled with [3H]leucine, [14C]fructose or [3H]glucosamine. The M(r) of this glycoprotein is lower than those of other HSV glycoproteins. Immunoassays of BHK cells infected with HSV-1-HSV-2 intertypic recombinants localized the gene encoding the target antigen of MAb CH-A9 to the unique long (UL) region at map units 0.490 to 0.564. Tunicamycin effectively inhibits N-linked glycosylation of g30K, which suggests that g30K may be modified by addition of N-linked oligosaccharides and that the amino acid sequence may contain Asn-X-Ser or Asn-X-Thr. The g30K was also purified on an immunoadsorbent column consisting of MAb CH-A9 linked to Sepharose 4B and was shown to be an HSV-2 type-specific antigen by indirect ELISA. The glycoprotein could induce HSV-2 type-specific neutralizing antibody in BALB/c mice. This evidence suggests that g30K may be a novel glycoprotein of HSV-2.