Adolescent ; Humans ; Male ; Neurofibroma, Plexiform ; Neurofibromatoses ; Parotid Neoplasms

The medicine for military use only is an essential material for medical support. The United States of America is one of the earliest countries which has used special medicine to protect the military personnel from injuries and diseases. The current situation of service support in the military of USA is introduced and the challenges facing the development, product, supply and use of the special medicine in USA are analyzed,for reference by our army.

AIM To explore the effects of Sangtong alkaloids (total alkaloids and total flavones from Mori folium,STA) on the random blood glucose,starch tolerance and hepatic insulin resistance in db/db mice with type 2 diabetes mellitus.METHODS Eight-week-old db/db mice were divided into model group (normal saline),acarbose group (39 mg/kg) and Sangtong alkaloids groups (105,210 and 420 mg/kg),db/m mice were used as control group (normal saline).The mice were given by intragastric administration for one hundred days.The random blood glucose of mice was determined every ten days.The starch tolerance was determined in the 100th day,together with the determination of serum insulin level,insulin resistance index and insulin sensitivity index.Histopathology changes of pancreas were observed by HE staining.Protein expressions of P-IRS1,P-PI3 K,P-AKT and GLUT2 were detected by Western blot.RESULTS Sangtong alkaloids significantly decreased the random blood glucose,serum insulin level and insulin resistance index,and increased the insulin sensitivity index in db/db mice.Meanwhile,Sangtong alkaloids ameliorated the pancreas histopathological damage and up-regulated the protein expressions of P-IRS1,P-PI3K,P-AKT and GLUT2 in liver.CONCLUSION Sangtong alkaloids can decrease the random blood glucose and improve the insulin resistance of liver in db/db mice with type 2 diabetes mellitus,whose mechanism may be associated with the regulation of hepatic insulin signal pathway.

BACKGROUNDThe underlying mechanism of early neurobiological impairment after subarachnoid hemorrhage (SAH) is not well understood, but the system of reactive oxygen superoxide (ROS) might be involved. Edaravone (MCI-186), a potent free radical scavenger that prevents apoptosis of neurons, was thus used in this study to see its possible therapeutic effect in early brain injury due to SAH in a rat model.

METHODSOne hundred and twenty male Sprague-Dawley rats were randomly assigned to four groups: group 1, control rats receiving sham operation only; group 2, rats with SAH treated by saline; group 3, rats with SAH treated with 1 mg/kg MCI-186 injected intraperitoneally; and group 4, rats with SAH treated with 3 mg/kg MCI-186. Treated with either saline or MCI-186 twice daily for two consecutive days after SAH, the rats were sacrificed for measurements of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) and histological analysis of caspase-3 protein by Western blotting and immunohistochemical staining. In addition, mortality and neurological scores were statistically analyzed by the chi-square test and Dunn's procedure respectively for each group. One-way analysis of variance followed by the Tukey's procedure was also used in data analysis.

RESULTSThe rats in group 2 that received saline only showed neurological impairment as well as elevated mortality, and were found to have significantly increased levels of MDA and caspase-3, but reduced SOD activities in brain tissues (P < 0.05). When treated with MCI-186 at two different dosages, the rats in groups 3 and 4 had markedly decreased levels of MDA and caspase-3 but increased SOD activities in the brain tissue (P < 0.05), along with improved scores of neurological evaluation (P < 0.05).

CONCLUSIONSThis study sheds some lights on the therapy of SAH-induced early brain injury by providing the promising data indicating that MCI-186, a radical scavenger, can efficiently diminish apoptosis of neurons and thus prevent the function loss of the brain in rats with SAH.

Animals ; Antipyrine ; analogs & derivatives ; therapeutic use ; Blotting, Western ; Brain Injuries ; drug therapy ; etiology ; Immunohistochemistry ; Male ; Malondialdehyde ; metabolism ; Neuroprotective Agents ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; physiopathology ; Superoxide Dismutase ; metabolism

Objective:Based on the regulatory effect of curcumin (Cur) on inflammation and iron death, to explore the mechanism of Cur protecting against cerebral ischemia-reperfusion injury (CIRI).Methods:A rat model of middle cerebral artery occlusion (MCAO) was established by the modified suture-occluded method. The modeled SD rats were randomly divided into the Sham group, CIRI group and Cur group. The neurobehavioral score of rats was measured by the Longa method. Hematoxylin-eosin (HE) staining was used to observe the pathological changes in the brain tissue of rats in each group. Furthermore, the contents of glutathione (GSH), malondialdehyde (MDA) and Fe 2+, as well as the levels of the inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in the ischemic cerebral cortex, were detected by corresponding testing kits. Western blotting was applied to detect the expression of glutathione peroxidase 4 (GPX4), a key regulatory protein of ferroptosis in the cerebral cortex. In addition, neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay, and ultrastructural changes in neurons in the cerebral cortex were observed under a transmission electron microscope. Results:Compared with the CIRI group, the Cur group showed decreased neurobehavioral scores, significantly reduced contents of MDA, Fe 2+, TNF-α, IL-1β and IL-6 (all P<0.05), but obviously increased content of GSH and protein expression of GPX4 (both P<0.05). Further pathological examination revealed edema, rupture and necrosis of neurons in the CIRI group, while mild edema and a small number of necrotic cells were observed in the Cur group only. The results of TUNEL staining indicated that the rate of neuronal apoptosis in the Cur group was lower than that in the CIRI group, with a statistically significant difference between groups [(23.6±3.5)% vs. (36.8±4.2)%; P<0.05]. In addition, under the transmission electron microscope, the CIRI group had a reduced volume of mitochondria, thickened double-layer membrane structure, and decreased or disappeared mitochondrial cristae, while the Cur group showed partial margination of nuclear chromatin and alleviated damage to mitochondria. Conclusions:Cur could attenuate CIRI, and its neuroprotective mechanism may be related to the inhibition of the inflammatory response and GPX4-mediated ferroptosis.

AIM To observe the effects of Sangtongjian Mixture (STJ) on glucose and lipid metabolism,insulin resistance and fat cytokines in type 2 diabetic rats,and their mechanisms of action.METHODS One hundred and forty rats fed on the combination of STZ and high fat diet were established as the type 2 diabetic models.Fasting blood glucose (FBG) level reached more than 16.7 mmol/L and then the rats were randomly divided into model group,metformin (180 mg/kg) group,STJ (73.5,147 and 294 mg/kg) groups.Ten rats were set as the blank group.Each treatment group was intragastrically given the corresponding agents for twelve weeks.The fasting blood glucose levels of rats were measured once every two weeks after the administration.After a 12-week administration period,glycosylated serum protein (GSP),glycosylated hemoglobin (GHb) and lipid profile indices (TC,TG,HDL-C and LDL-C) were determined.The serum insulin level was measured by radioimmunoassay,and homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity index (ISI) were calculated.The levels of serum adiponectin and leptin were detected by ELISA.RESULTS STJ remarkably decreased the levels of FBG,GSP,GHb,TC,TG,LDL-C,leptin and HOMR-IR in type 2 diabetic rats.Furthermore,STJ also significantly increased the levels of HDL-C,adiponectin and ISI.CONCLUSION STJ can improve glucose and lipid metabolism in type 2 diabetic rats by ameliorating insulin resistance and regulating fat cytokine levels.