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Chinese Journal of Experimental Traditional Medical Formulae ; (24): 125-129, 2019.
Article in Chinese | WPRIM | ID: wpr-802309

ABSTRACT

Objective:To observe clinical efficacy of Shengma Biejia Tang combined with Shenfutang on sepsis-induced myocardial dysfunction (SIMD) and study the controlling effect on inflammatory reaction. Method:Eighty-eight patients with SIMD were randomly divided into control group (44 cases) and observation group (44 cases) by random number table. Patients in control group received the early bundle therapy of sepsis, including fluid resuscitation, anti-infection treatment and vasoactive drugs. In addition to the therapy of control group, patients in observation were also given Shengma Biejia Tang combined with Shenfutang, 1 dose/day. And a course of treatment was 7 days. Before and after treatment, levels of troponin (cTnI), creatine kinase isoenzyme (CK-MB), N terminal brain natriuretic precursor (NT-proBNP), calcitonin (PCT), hypersensitivity C reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), interleukins-6 (IL-6) and blood lactic acid (LAC) were detected. And color Doppler ultrasound examination of the heart was performed to record left ventricular ejection fraction (LVEF), blood flow velocity of early mitral valve diastole and ratio of blood flow velocity at atrial systolic peak (E/A) and stroke volume (SV). And lactate clearance rate (LCR) was calculated. And sequential (sepsis-related) organ failure assessment (SOFA), acute physiology and chronic health (APACHEⅡ) and traditional Chinese medicine(TCM)syndromes were scored. Result:After treatment, levels of cTnI, NT-ProBNP, CK-MB, Hs-CRP, IL-6, PCT, TNF-α and LAC in observation group were lower than those in control group (PPPConclusion:In addition to the integrated western medicine, Shengma Biejia Tang combined with Shenfutang can control inflammatory reaction, relieve myocardial inhibition and myocardial damage, and protect and improve heart function, and alleviate the symptoms.

2.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 13-18, 2019.
Article in Chinese | WPRIM | ID: wpr-801859

ABSTRACT

Objective:To investigate the relationship between NOD-like receptor pyrin domain containing 3(NLRP3)/cysteine aspartate-specific protease(Caspase)-1 signaling pathway and esophageal inflammation by observing the effect of Xuanfu Daizhe Tang on the composition of inflammatory body and the expression of relevant inflammatory factors in rats with reflux esophagitis (RE), so as to explain the mechanism of Xuanfu Daizhe Tang in treating RE. Method:Sixty healthy male Wistar rats were randomly divided into four groups:the normal control group, the model control group, the Xuanfu Daizhe Tang group (9.89 g·kg-1) and the positive control group (omeprazole enteric-coated tablets+mosapride, 2.58 mg·kg-1), with 15 rats in each group. Except for the blank control group, the remaining rats were operated by " 4.2 mm pyloric clip+2/3 gastric fundus ligation" to establish models. Since the 8th day after the operation, the rats were given corresponding drugs twice a day for 14 days. The arterial blood and esophageal tissues were taken out at the 15th day after the intervention. The pathological morphology of esophagus was observed by naked eyes and under light microscopy. The secretion of cytokines Caspase-1 and interleukin(IL)-1β in serum was detected by enzyme linked immunosorbent assay(ELISA). The expressions of NLRP3, Caspase-1 and IL-1β in esophagus were detected by Western blot. Result:Compared with the normal group, the injury of esophageal mucosa in the model group was the most serious. Compared with the normal group, the levels of Caspase-1 and IL-1β in serum and the expression of NLRP3 protein in esophageal tissue of the model group were significantly increased (PPβ in serum of rats, and down-regulate the expressions of NLRP3, Caspase-1 and IL-1β protein in esophageal tissue (P0.05, PConclusion:Xuanfu Daizhe Tang can regulate the expressions of NLRP3 and Caspase-1, and reduce the content of IL-1β, suggesting that it may antagonize esophageal inflammatory response, reduce esophageal inflammatory injury and treat RE by inhibiting the activation of NLRP3/Caspase-1 signaling pathway.

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