Kondrupandreassen7919

Our findings suggest that hypertension can be treated using THPs. However some THPs can counteract treatment of hypertension. Further studies should be developed on use of THPs for treatment of hypertension are critical, and guidelines for use of traditional herbal medicines to treat hypertension.

To evaluate the efficacy of Shenfu decoction (SFD) prepared with a traditional Chinese formula, on sepsis in rats with the condition induced by cecal ligation and puncture (CLP), and to study the possible mechanism underlying its action.

Forty clean-grade male Sprague-Dawley rats were divided randomly into three groups normal control group (NCG, n = 10), model control group (MCG, n = 15) and Shenfu decoction group (SFDG, n = 15). Sham-operated rats in NCG were served as operation control, while rats in both MCG and SFDG were exposed to CLP, a procedure to develop experimental sepsis. Rats in SFDG were administered with SFD by gavage (3 mg/g of body weight, twice a day) 2 h prior to CLP and directly after successful CLP, while rats in NCG and MCG were gavaged with equivalent volume of sterilized water. Rats in all groups were starved with free access to drink. After 24 h of administration, the mortality of rats in each group was assessed. The indicators of inflammatory response [the peritoneal inflammationduced by sepsis were observed, and these two disturbed gut microbiota phyla could be regulated after SFD treatment. Increase in levels of Proteobacteria and reduction levels of Bacteroidetes induced by sepsis were observed, and these two disturbed gut microbiota phyla could be regulated after SFD treatment.

SFD may play a protective role in sepsis by alleviating sepsis-induced inflammatory response and gut barrier damage in rats.

SFD may play a protective role in sepsis by alleviating sepsis-induced inflammatory response and gut barrier damage in rats.

To determine the effect of Wenyang Huazhuo Fang (WHF), a Traditional Chinese Medicine decoction, on renal function in a rat model of doxorubicin-induced nephropathy, and to elucidate the underlying mechanism.

Sprague-Dawley rats were randomly divided into six groups control, doxorubicin-nephropathy, and prednisone-treated (6.45 mg·kg-1·d－1) doxorubicin nephropathy groups, as well as high- (7.26 g·kg-1·d－1, medium- (2.42 g·kg-1·d－1, and low-dose (0.81 g·kg-1·d－1 WHF-treated doxorubicin-nephropathy groups. The nephropathy rat model was established by two tail vein injections of doxorubicin, followed by prednisone or WHF treatment for 8 weeks. Body weights were monitored and urinary protein was measured every 2 weeks. After the end of the treatment period, the rats were euthanized. Serum biochemical indicators were determined and renal morphological alterations were assessed using histological staining. The expression of transient receptor potential cation channel subfamily C member 6 (TRPC6), stromal interaction molecule 1 (STIM1), and calcium release-activated calcium channel protein 1 (Orai1) was detected using western blotting, and their mRNA levels were examined using quantitative real-time reverse transcription-polymerase chain reaction.

WHF treatment was found to significantly ameliorate weight loss, proteinuria, hypoalbuminemia, and dyslipidemia in doxorubicin-nephropathy rats. The protein and mRNA levels of TRPC6, STIM1, and Orai1 were partially, but significantly suppressed by prednisone or WHF treatment.

Treatment with WHF significantly ameliorates renal injury in a rat model of doxorubicin-induced nephropathy, which could be at least partially related to repression of the TRPC6 pathway.

Treatment with WHF significantly ameliorates renal injury in a rat model of doxorubicin-induced nephropathy, which could be at least partially related to repression of the TRPC6 pathway.

To dynamically observe the efficacy of Jieduan Niwan formula (JDNW) on a rat model of acute-on-chronic liver failure (ACLF).

Seventy Wistar rats were divided into control group (6 rats), model group (22 rats), JDNW group (21 rats), and SP600125 group (21 rats). 13 weeks' porcine serum injection followed with D-galactosamine and lipopolysaccharide joint acute attack was used to establish ACLF model. Rats in JDNW group were orally given JDNW formula for 3 days before acute attack; rats in SP600125 group were injected with SP600125 30 min ahead of acute attack. buy ML265 Rats were sacrificed respectively at 4, 8 and 12 h after model established. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), Creatinine (CR), blood urea nitrogen (BUN), prothrombin activity (PTA) were examined by biochemical process, Tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), transformed growth factor-beta 1 (TGF-β1), High mobility group box-1 (HMG levels (P < 0.05), moreover, the AI and expression of p-JNK, Bax, Bad, Bid and Cyt C were lower than model group at 4 and 8 h but were higher at 12 h (P < 0.05). Similar results were observed in SP600125 group.

An ACLF rat model with low mortality can be established by porcine serum joint with D-galactosamine + lipopolysaccharide induction; JDNW decoction can effectively suppress the inflammatory reaction, improve the immune system, and protect the liver of ACLF rats, the mechanism might involve the inhibition of the JNK-induced mitochondrial apoptotic pathway.

An ACLF rat model with low mortality can be established by porcine serum joint with D-galactosamine + lipopolysaccharide induction; JDNW decoction can effectively suppress the inflammatory reaction, improve the immune system, and protect the liver of ACLF rats, the mechanism might involve the inhibition of the JNK-induced mitochondrial apoptotic pathway.

To study the effect of Bushen Jiangzhi formula (BSJZF) on atherosclerosis (AS) in apolipoprotein E knockout (apoE-/-) mice and the underlying mechanism.

We used a high fat diet to induce AS in apoE-/- mice. The mice were randomly divided into four groups model, BSJZF, atorvastatin, and 3-methyladenine groups. Syngeneic C57BL/6 mice of the same age were used for the control group. Autophagosomes in the aorta were examined by transmission electron microscopy. Morphology, lipid accumulation, and collagen deposition in the aorta were examined by hematoxylin and eosin, Oil Red O, and Masson's staining, respectively. Serum levels of tumor necrosis factor alpha (TNF-), interferon gamma (IFN-), and interleukin 10 (IL-10) were measured by enzyme-linked immunoassays. Protein expression of microtubule-associated protein light chain 3 (LC3), Beclin 1, and p62 in the aorta were examined by Western blot analyses.

ApoE-/- mice fed a high fat diet exhibited AS symptoms including less autophagosomes in the aorta, higher serum levels of TNF-a, IFN-r, and p62, and lower serum levels of IL-10, LC3, and Beclin 1.