Ginsenoside Rg1 attenuates liver injury induced by D-galactose in mice.

The present study investigated the effect and underlying mechanisms of ginsenoside Rg1 (Rg1) in attenuating subacute liver injury induced by D-galactose (D-gal) in mice. Specific Pathogen Free (SPF) male C57BL/6J mice were randomly divided into 3 groups: i) D-gal-administration group (D-gal group), where the mice were intraperitoneally administrated with D-gal (120 mg/kg/day for 42 days); ii) D-gal + Rg1 group where the mice were treated with 120 mg/kg/day D-gal for 42 days and with Rg1 at a dose of 20 mg/kg/day for 35 days. The first dose of Rg1 was administered on the 8th day of treatment with D-gal; and iii) the normal control group, where the mice were injected with an equal volume of saline for 42 days. The day following the final injections in all groups, peripheral blood was collected and serum was prepared to measure the contents of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TBiL), advanced glycation end products (AGEs) and 8-hydroxy-2 deoxyguanosine (8-OH-dG). Liver tissue homogenates were prepared to measure the contents of malondialdehyde (MDA) and glutathione (GSH), and the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). Paraffin section were prepared to observe the microscopic structure of the liver. Transmission electron microscopy was used to observe the ultrastructure of hepatocytes. Frozen section were prepared and stained with senescence-associated ß-galactosidase to detect the relative optical density value of senescence-associated markers. Compared with the D-gal group, the contents of AST, ALT, TBiL, AGEs and MDA significantly decreased in the D-gal + Rg1 group, while the activities of SOD and GSH-Px markedly increased, and liver injury and degenerative alterations of hepatocytes were reduced. Administration of Rg1 induced a protective effect on D-gal-induced liver injury in mice by inhibiting the oxidative stress, reducing DNA damage and decreasing the AGE content.

Role of endoplasmic reticulum stress signaling pathway in high fat-induced cell apoptosis in vascular endothelial cells / 中国药理学通报

Aim To explore the role of endoplasmic reticulum stress(ERS)signaling pathway in high fat-induced cell apoptosis in human umbilical vein endo-thelial cells(HUVECs). Methods HUVECs were ex-posed to different concentrations of palmitic acid(0. 1, 0. 2,0. 4,0. 8 mmol·L - 1 )for 24 h and different time points of 0. 4 mmol·L - 1 palmitic acid(0,12, 24,48 h). Cell viability was measured by cell count-ing kit(CCK-8),and the protein expressions of ERS signaling pathway protein such as GRP78,CHOP, PERK,IRE1,ATF6 were determined by Western blot. The level of intracellular apoptosis was detected by immunofluorescence. Results HUVECs exposed to palmitic acid at 0. 4 mmol·L - 1 for 24 h showed a de-crease in their viability and an increase in the expres-sion of ERS signaling pathway proteins (GRP78, CHOP,PERK,IRE1,ATF6)(P < 0. 05);cell ap-optotic levels significantly increased(P < 0. 05). The intracellular apoptosis levels in the vascular endothelial cells of ERS signaling pathway inhibitor 4-phenylbutyr-ic acid (4-PBA,10 mmol · L - 1 )were significantly lower than those of the PA group(P < 0. 05). Conclu-sion Activated ERS signaling pathway might play an important role in the treatment of high fat-induced cell apoptosis in vascular endothelial cells.

Role of NADPH oxidase in high fat-induced oxidative stress injury in human umbilical vein endothelial cells / 中国药理学通报

Aim To explore the role of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in high fat-induced oxidative stress injury in human umbilical vein endothelial cells (HUVECs).Methods HUVECs were exposed to different concentrations of palmitic acid(0.1,0.2,0.4,0.8 mmol · L-1) for 24 h and different time points of 0.4 mmol · L-1 palmitic acid(0,12,24,48 h).Cell viability was measured by Cell Counting Kit 8,and the protein expression of NADPH oxidase subunits such as p22phox,p47phox,p67phox and gp91phox were determined by Western blot.The expression of reactive oxygen species (ROS) in HUVECs was detected by immunofluorescence.Results Cell proliferation rate of HUVECs stimulated by 0.4 mmol · L-1 palmitic acid for 24 h and 48 h was significantly reduced.In the next experiment,model group was accordingly set as HUVECs stimulated by 0.4 mmol · L-1 palmitic acid for 24 h.The expression of NADPH oxidase subunits such as p22phox,p47phox,p67phox and gp91phox significantly increased at 24 h and 48 h after 0.4 mmol· L-1 palmitic acid stimulation (P ＜ 0.05),and the difference.between the 24 h group and the 48 h group was not significant (P ＞ 0.05).The expression of ROS in HUVECs significantly increased at 24 h and 48 h after O.4 mmol · L-1 palmitic acid stimulation (P ＜ 0.05),and the difference between 24 h group and 48 h group was not significant (P ＜ 0.05).Compared with the model group (0.4 mmol · L-1 palmitic acid stimulation for 24 h),the NADPH oxidase inhibitor diphenyliodonium (DPI,10 μmol · L-1) pretreatment could significantly decrease the expression of ROS in vascular endothelial cells (P ＜ 0.05).Conclusion Activated NADPH oxidase might play an important role in treatment of high fat-induced oxidative stress injury in vascular endothelial cells.

[Distraction osteogenesis in correcting facial asymmetry malformation caused by temporomandibular joint ankylosis: a case report].

A facial asymmetry patient caused by temporomandibular joint ankylosis was operated by putting a distraction osteogenesis (DO)-appliance. One week after surgery, the right mandible was distracted. Twenty days after distraction, the height of right mandibular ramus and body increased obviously. Four months after retain of DO-appliance, the right maxilla down-grew automatically and the occluding relation recovered to normal. The DO-appliance was taken out. MEDPOR prosthesis was imbedded in new bone and genioplasty was operated. The facial asymmetry and abnormal occluding relation of the patient were improved obviously.