Objective:To investigate EB PAOA's effects on the level of cytokines produced by the mice transplanted with S 180 cells and induction actions for apoptosis of colon cancer CL 187 cells so as to probe into EB PAOA's antineoplastic active mechanism preliminarily Methods:MTT assay was used to detect EB PAOA's effects on the level of cytokines,including IL 2?IFN ??IL 1 and TNF ?,produced by the mice transplanted with S 180 cells Then, human colon cancer CL 187 cell strains were cultured in vitro and MTT assay was adopted to determine the inhibition rate to CL 187 cells Apoptotic cells were observed and confirmed with an electronmicrograph Apoptotic rate were then detected through a flow cytometer Results:The ability of the mice transplanted with S 180 cells to produce IL 2?IL 1 and TNF ? after treated with EB PAOA was strengthened EB PAOA can inhibit the proliferation of CL 187 cells Large number of apoptotic cells were found under the electronmicrograph There was an apoptotic peak appeared in DNA histogram of the flow cytometer The apoptotic rate was of time dependent.Conclusion:The antineoplastic mechanism of EB PAOA may be realized by stimulating the splenocytes of the mice transplanted with S 180 cells to secrete IL 2 and macrophages to secrete IL 1 and TNF ? to strengthen cellular immune functions and induce the apoptosis of tumor cells directly

Bibenzyl is a type of active compounds abundant in Dendrobium. In the present study, we investigated the inhibitory effects of six bibenzyls isolated from Dendrobium species on vascular endothelial growth factor (VEGF)-induced tube formation in human umbilical vascular endothelial cells (HUVECs). All those bibenzyls inhibited VEGF-induced tube formation at 10 micromol x L(-1) except tristin, and of which moscatilin was found to have the strongest activity at the same concentration. The lowest effective concentration of moscatilin was 1 micromol x L(-1). Further results showed that moscatilin inhibited VEGF-induced capillary-like tube formation on HUVECs in a concentration-dependent manner. Western blotting results showed that moscatilin also inhibited VEGF-induced phosphorylation of VEGFR2 (Flk-1/KDR) and extracellular signal-regulated kinase 1/2 (ERK1/2). Further results showed that moscatilin inhibited VEGF-induced activation of c-Raf and MEK1/2, which are both upstream signals of ERK1/2. Taken together, results presented here demonstrated that moscatilin inhibited angiogenesis via blocking the activation of VEGFR2 (Flk-1/KDR) and c-Raf-MEK1/2-ERK1/2 signals.

The cardioprotective effects of melatonin on recovery of rat donor hearts after 12 h of preservation were investigated. Wistar rats weighing 200 to 250 g (n=24) were randomly divided into 3 groups. In the non-storage group (n=8), donor hearts were not stored. In the melatonin group (n=8), donor hearts were stored in 4 degrees C St. Thomas solution with melatonin (0.1 mmol/L). In the control group (n=8), donor hearts were stored in 4 degrees C St. Thomas solution only. The coronary flow (CF), cardiac function, coronary vasodilatory response, creatine kinase (CK) and high energy phosphate levels were measured after the hearts had been preserved for 12 h. Transmission electron microscopy was used to examine the microstructural changes after 12 h of preservation. The recovery of cardiac function and coronary vasodilatory response were significantly improved in the melatonin group (P<0.01). CK release decreased greatly in the melatonin group (P<0.01). High energy phosphate levels were significantly better preserved in the melatonin group (P<0.01). Histological findings were much better in the melatonin group than in the control group. These results suggest that melatonin has cardioprotective effects on the recovery of rat donor hearts after 12 h of preservation.
Animals ; Cardiotonic Agents ; pharmacology ; Creatine Kinase ; metabolism ; Free Radical Scavengers ; pharmacology ; Heart Transplantation ; Humans ; Hydroxyl Radical ; Male ; Melatonin ; pharmacology ; Myocardial Reperfusion Injury ; prevention & control ; Myocardium ; metabolism ; ultrastructure ; Organ Preservation ; methods ; Random Allocation ; Rats ; Rats, Wistar ; Time Factors

Colorectal cancer is a common digestive system malignant tumor in the world, its incidence and mortality rate is in the forefront, with the social progress and the change of diet structure, the incidence of colorectal cancer is gradually increasing, and there is a trend of younger age. Among them, peritoneal metastasis is the main cause of death in patients with colorectal cancer. Non-surgical treatment has been used in the past, but the prognosis is poor. How to treat and prevent peritoneal metastasis in colorectal cancer patients and improve the prognosis of such patients as much as possible is a question worth our in-depth study. The hyperthermic intraperitoneal chemotherapy provides a new direction for the treatment of colorectal cancer patients, usually combined with surgical treatment, and co-applied in the clinic as a new treatment model. This article reviews the treatment mode of hyperthermic intraperitoneal chemotherapy, the choice of drugs, and the progress of research in the treatment and prevention of peritoneal metastasis in colorectal cancer.

Hepatic fibrosis is a common complication of chronic liver disease， seriously affecting patients' quality of life and leading to severe consequences such as cirrhosis and liver cancer. Modern medicine has made progress in the treatment of hepatic fibrosis， while it still faces certain challenges and limitations. Therefore， seeking new therapeutic strategies is of great clinical significance. The nuclear factor-κB （NF-κB） signaling pathway plays a role in regulating inflammation and immune responses. Recent studies have shown that the NF-κB signaling pathway plays a key role in the occurrence and development of hepatic fibrosis. The abnormal activation of the NF-κB signaling pathway leads to the overexpression of genes related to liver inflammation and fibrosis， thereby promoting the development of hepatic fibrosis. Traditional Chinese medicine （TCM） is a traditional treatment method with unique advantages and potential. In recent years， increasing studies have proved that TCM can treat hepatic fibrosis by regulating the NF-κB signaling pathway. The active ingredients in Chinese herbal medicines can intervene in the activation of the NF-κB signaling pathway to inhibit inflammatory responses， thereby reducing the severity of hepatic fibrosis. This article reviews the mechanisms of TCM in treating hepatic fibrosis via the NF-κB signaling pathway and evaluates the efficacy and discusses the clinical application prospects of relevant Chinese herbs and formulae， aiming to provide references for further research and clinical practice.

ObjectiveTo observe the effects of Tongmai Kaiqiao pills on the hypoxia-inducible factor-1α （HIF-1α）/adenovirus E1B 19 kD-interacting protein 3 （BNIP3） signaling pathway and mitochondrial autophagy in the hippocampus of the rat model of vascular dementia （VD）. MethodNinety male SD rats underwent adaptive feeding for one week before the study. Ten rats were randomly assigned to the sham group， where the common carotid artery was isolated without ligation. The remaining rats were subjected to sequential ligation of the common carotid artery for the modeling of VD. The successfully modeled rats were randomly assigned into the following groups： model， high-， medium-， and low-dose （27.6， 13.8， 6.9 g·kg^-1， respectively） Tongmai Kaiqiao pills， donepezil hydrochloride （0.45 mg·kg^-1）， and combination （27.6 g·kg^-1 Tongmai Kaiqiao pills + 2.5 mg·kg^-1 HIF-1α inhibitor YC-1） groups. After 4 weeks of treatment， samples were collected. Nissl staining and hematoxylin-eosin staining were performed to observe the loss of neurons and pathological changes， respectively， in the hippocampal region. Western blot was employed to determine the protein levels of HIF-1α， BNIP3， Beclin-1， and microtubule-associated protein 1 light chain 3B （LC3B） in the hippocampal tissue. Transmission electron microscopy was used to observe the mitochondrial ultrastructure and the number of autophagosomes in the hippocampal tissue. Immunofluorescence was employed to observe the fluorescence intensity of HIF-1α， BNIP3， and LC3B in the hippocampal tissue. ResultCompared with the sham group， the model group showed prolonged escape latency （P<0.01）， decreased number of platform crossings （P<0.01）， reduced and disarranged neuronal layers in the hippocampal region， decreased number of Nissl bodies， disrupted mitochondrial cristae， damaged mitochondrial double-membrane structures， increased number of autophagosomes， upregulated expression of HIF-1α， BNIP3， beclin1， and LC3B （P<0.05， P<0.01）， and enhanced fluorescence intensity of HIF-1α， BNIP3， and LC3B （P<0.05， P<0.01）. Compared with the model group， Tongmai Kaiqiao pills and donepezil hydrochloride shortened the searching time for the platform （P<0.01） and increased the number of platform crossings （P<0.01）. Moreover， the drugs increased the number of neurons with normal morphology and orderly arrangement and the number of Nissl bodies， alleviated the damage， increased the number of autophagosomes， upregulated the expression of HIF-1α， BNIP3， Beclin1， and LC3B （P<0.05， P<0.01）， and enhanced the fluorescence intensity of HIF-1α， BNIP3， and LC3B （P<0.05， P<0.01）. Compared with high-dose Tongmai Kaiqiao pills， the combination group prolonged the escape latency （P<0.01）， reduced the number of crossing platforms （P<0.01）， decreased the number of hippocampal neurons， aggravated the damage， decreased the number of Nissl bodies and autophagosomes， downregulated the expression of HIF-1α， BNIP3， beclin1， and LC3B （P<0.01）， and decreased the fluorescence intensity of HIF-1α， BNIP3， and LC3B （P<0.01）. ConclusionTongmai Kaiqiao pills may activate the HIF-1α/BNIP3 signaling pathway to promote the occurrence of mitochondrial autophagy， clear damaged mitochondria， provide energy for healthy cells， reduce neuronal cell death， and restore the brain function， thereby reducing ischemic damage to the hippocampal tissue， improving learning and memory abilities， and exerting therapeutic effects on VD in rats.