ABSTRACT
OBJECTIVE: The effects of butylphthalide on serum C-reactive protein (CRP), Parkinson disease protein 7 (PARK7), and neurotrophin-3 (NT-3) levels, and neurological function in patients with acute cerebral infarction (ACI) were explored in order to provide a reference for clinical treatment of the disease. METHODS: One hundred and twenty patients with ACI treated in our hospital from September 2016 to June 2018 were selected and randomized into the control group and the study group, with 60 cases in each group. Patients in the control group were treated with conventional therapy, while those in the study group were treated with butylphthalide. Clinical efficacy, serum levels of CRP, PARK7, and NT-3, as well as the scores of National Institutes of Health Stroke Scale (NIHSS), Fugl-Meyer Assessment (FMA), and Barthel Index (BI) before and 2 months after treatment were analyzed and compared between the two groups. RESULTS: The study group had a significantly higher effective rate (93.33%) than the control group (73.33%; P<0.05). Before treatment, differences in serum CRP, PARK7, NT-3, IL-6, IL-8, and IL-10 levels between the study group and the control group were barely notable (P>0.05). After treatment, the study group observed lower serum levels of CRP, PARK7, IL-6, IL-8, and a higher levels of IL-10, NT-3 in comparison with those of the control group (P<0.05). Before treatment, NIHSS, FMA, and BI scores between the two groups did not show significant differences (P>0.05). After treatment, the study group yielded a remarkably lower NIHSS score and higher FMA and BI scores than the control group (P<0.05). CONCLUSION: Butylphthalide is effective in the treatment of ACI. It can effectively facilitate the recovery of neurological and motor functions of patients, enhance their quality of life and improve serum CRP, PARK7, and NT-3 levels, which is worthy of clinical promotion.
ABSTRACT
The specific and efficient activation of mitogen-activated protein kinase (MAPK) signaling modules is mediated, at least in part, by scaffold proteins. c-Jun NH(2)-terminal kinase (JNK)-associated leucine zipper protein (JLP) was identified as a scaffold protein for JNK and p38 MAPK signaling modules. JLP is expressed nearly ubiquitously and is involved in intracellular signaling pathways, such as the G(alpha13) and Cdo-mediated pathway, in vitro. To date, however, JLP expression has not been analyzed in detail, nor are its physiological functions well understood. Here we investigated the expression of JLP in the mouse testis during development. Of the tissues examined, JLP was strongest in the testis, with the most intense staining in the elongated spermatids. Since the anti-JLP antibody used in this study can recognize both JLP and sperm-associated antigen 9 (SPAG9), a splice variant of JLP that has been studied extensively in primates, we also examined its expression in macaque testis samples. Our results indicated that in mouse and primate testis, the isoform expressed at the highest level was JLP, not SPAG9. We also investigated the function of JLP by disrupting the Jlp gene in mice, and found that the male homozygotes were subfertile. Taken together, these observations may suggest that JLP plays an important role in testis during development, especially in the production of functionally normal spermatozoa.
