Influence of Tangshenfang on diabetic liver injury and the expression of SIRT1 and PGC-1αin the liver tissue / 中国病理生理杂志

AIM:To observe the effect of Tangshenfang(TS)on the liver protection and the levels of silent in-formation regulator 1(SIRT1)and peroxisom proliferator-activated receptor γcoactivator-1α(PGC-1α)in the liver tissue. METHODS:The rat model of diabetes mellitus(DM)was established by intravenous injection of streptozotocin(STZ;30 mg/kg)after having the high fat/high glucose diets for 1 month.The diabetic rats were randomly divided into DM group,DM with high-dose TS(TSHi)group, medium-dose TS(TSMed)group and low-dose TS(TSLow)group.The normal rats were served as control group.There were 8 rats in each group.After treatment with TS for 12 weeks,the serum biochemical indi-ces including fasting blood glucose(FBG), triglyceride(TG), alanine aminotransferase(ALT)and aspartate aminotrans-ferase(AST)were tested.Fasting insulin(FINS)was also detected by radioimmunoassay,and homeostatic model assess-ment for insulin resistance(HOMA-IR)was calculated.The serum levels of tumor necrosis factor-α(TNF-α)and interleu-kin-1(IL-1)were measured by ELISA.The activity of SOD and content of MDA in the liver tissues were measured by the methods of hydroxylamine and thiobarbituric acid.The liver pathological changes were observed under light microscope with HE and Masson staining.The protein expression of SIRT1and PGC-1αin the liver tissues was determined by Western blot. RESULTS:In DM group,serum FBG,TG,ALT,AST,FINS,HOMA-IR,TNF-αand IL-1 were obviously increased com-pared with the control group(P<0.01).The fatty changes,local necrosis,inflammation and fibrosis in the liver tissues were observed.The content of MDA in liver increased,while the activity of SOD decreased markedly.The protein expression of SIRT1 and PGC-1αwas decreased(P<0.05).In TS treatment groups,all these changes in DM rats were markedly reversed by TS,and the protein expression of SIRT1 and PGC-1αin the liver tissues was markedly increased.CONCLUSION:TS may protect the rats from diabetic liver injury by increasing the expression of SIRT 1 and PGC-1α,and thereby improving in-sulin resistance and oxidative stress.

Panax notoginseng saponins protect kidney from diabetes by up-regulating silent information regulator 1 and activating antioxidant proteins in rats / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore the mechanism of the protective effects of Panax notoginseng saponins (PNS) on kidney in diabetic rats.</p><p><b>METHODS</b>Diabetic rat model was obtained by intravenous injection of alloxan, and the rats were divided into model, PNS-100 mg/(kg day) and PNS-200 mg/(kg day) groups, 10 each. Another 10 rats injected with saline were served as control. Periodic acid-Schiff staining and immunological histological chemistry were used to observe histomorphology and tissue expression of bone morphogenetic protein-7 (BMP-7). Silent information regulator 1 (SIRT1) was silenced in rat mesangial cells by RNA interference. The mRNA expressions of SIRT-1, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor-1 (PAI-1) were analyzed by reverse transcription polymerase chain reaction. The protein expressions of SIRT1 and the acetylation of nuclear factor κB (NF-κB) P65 were determined by western blotting. The concentration of MCP-1, TGF-β1 and malondialdehyde (MDA) in culture supernatant were detected by enzyme-linked immuno sorbent assay. The activity of superoxide dismutase (SOD) was detected by the classical method of nitrogen and blue four.</p><p><b>RESULTS</b>In diabetic model rats, PNS could not only reduce blood glucose and lipid (P<0.01), but also increase protein level of BMP-7 and inhibit PAI-1 expression for suppressing fibrosis of the kidney. In rat mesangial cells, PNS could up-regulate the expression of SIRT1 (P<0.01) and in turn suppress the transcription of TGF-β1 (P<0.05) and MCP-1 (P<0.05). PNS could also reverse the increased acetylation of NF-κB p65 by high glucose. In addition, redox regulation factor MDA was down-regulated (P<0.05) and SOD was up-regulated (P<0.01), which were both induced by SIRT1 up-regulation.</p><p><b>CONCLUSIONS</b>PNS could protect kidney from diabetes with the possible mechanism of up-regulating SIRT1, therefore inhibiting inflammation through decreasing the induction of inflammatory cytokines and TGF-β1, as well as activating antioxidant proteins.</p>

The Correlation of Normal Adult Mastoid Pneumatization Volume and the History of Otitis Media in Childhood / 听力学及言语疾病杂志

Objective To explore the volume size of mastoid pneumatization in normal adults and the relation‐ship with a history of recurrent otitis media in childhood .Methods A total of in 40 adults (80 ears) ,based on with or without otitis media in childhood ,were divided into the study group (n= 20) and the control group (n=20) . The volume sizes of mastoid pneumatization were measured by temporal bone CT scanning of three-dimensional re‐construction ,and the relationship with the history of childhood ear infections was studied .Results The average vol‐ume of pneumatization in all 80 temporal bones was 10 .4 ± 1 .8 ml .The average volume of pneumatization in sub‐jects without otitis media history (48 ears) and subjects with a history of otitis media (32 ears) were 9 .7 ± 2 .2 ml and 6 .3 ± 1 .7 ml ,respectively .The difference was statistically significant (P0 .05) .Conclusion The volumes of mastoid pneumatization in normal ears have a wide range .The subjects with a history of recurrent otitis media in childhood may be the cause of the volume decrease of mastoid pneumatization in adulthood .