ABSTRACT
Objective To evaluate the efficacy of potassium sodium dehydroandroan drographolide succinate (PSDS) combined with routine therapy for rotavirus enteritis in children.MethodsA total of 148 children with rotavirus enteritis were included and divided into an observation group and a control group by random number table method, 74 in each group. The children in the observation group were treated with intravenous PSDS combined with routine therapy, and those in the control group with intravenous ribavirin combined with routine therapy. Serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay, and plasma lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase-MB (CK-MB) were determined using standard clinical laboratory procedures. The clinical efficacy was evaluated. Results The total efficacy rate in the observation group was significantly higher than that in the control group (91.9%vs. 78.4%;χ2=2.314,P<0.05). After the treatment, the serum levels of IL-6 (18.24 ± 3.62 ng/mlvs. 25.36 ± 5.25 ng/ml; t=2.425,P<0.05) and TNF-α (20.86 ± 4.28 ng/mlvs. 31.22 ± 7.15 ng/ml;t=2.503,P<0.05), and the plasma levels of LDH (104.25 ± 22.06 U/Lvs. 150.26 ± 37.22 U/L;t=2.316,P<0.05), CK (84.25 ± 13.57 U/Lvs. 107.88 ± 16.28 U/L;t=2.327,P<0.05) and CK-MB (22.30 ± 4.24 U/Lvs. 32.26 ± 7.14 U/L;t=2.426,P<0.05) in the observation group was significantly lower than those in the control group. The time to diarrhea resolution (2.42 ± 0.53 dvs.3.56 ± 0.78 d;t=2.316,P<0.05) and the time to fever resolution(2.11 ± 0.32 dvs.2.63 ± 0.43 d;t=2.472,P<0.05) in the observation group were significantly delayed than those in the control group, and the hospital length of stay longer (6.23 ± 1.42 dvs. 4.35 ± 0.96 d;t=2.413,P<0.05).Conclusions PSDS combined with routine therapy may reduce inflammatory response, protect from myocardial injury, and promote recovery in children with RVE.
ABSTRACT
The interaction betweenYan-Hu-Ning (YHN) and bovine serum albumin (BSA) was investigated in order to provide further theoretical evidences on action mechanism study between YHN and proteins within the organism. Under optimal conditions, the interaction between YHN and BSA was studied by fluorescence quenching, ultraviolet absorption spectrometry and synchronous fluorescence spectroscopy. At the temperature of 283.15 K, 298.15 K and 313.15 K, quenching constant (KSV) and speed constant (Kq) were calculated by S-V curves. Static quenching constant (KLB) was obtained by L-B double reciprocal equation. Double logarithmic equation was used to calculate the binding constants (Kb) and the number of binding site (n). Thermodynamic equation was used to obtainΔH,ΔS,ΔG. Hill’s coefficients (nH) was obtained by Hill equation. The results showed that at three different temperatures, along with the increasing of YHN concentration, the fluorescence intensity of BSA decreased regularly. The value of KSV, Kq, KLB, Kb, n and nH decreased with the increasing of temperature;ΔG 1. It was concluded that YHN-BSA complex quenched the intrinsic fluorescence of BSA. The mechanism of fluorescence quenching was static quenching. The main binding forces were deduced as hydrogen bonds and Van der Waals forces from calculated values of thermodynamic parameters. YHN and BSA can form a binding site, which indicated certain binding interaction between YHN and BSA. YHN can be stored and transported by protein within the body. Free energy was produced to transformΔG into negative value. It showed that the process of binding between YHN and BSA was spontaneous. The nH was more than 1. It indicated that YHN had positive cooperative effect. The primary binding site was located at subdomainⅡA. The synchronous fluorescence spectra showed certain influence on the conformation of BSA by YHN. It led to the weakening of polarity within BSA and the binding site to be closer to the tyrosine.