Objective To investigate the change of apoptosis and drug resistance after multiple thermotherapy On the HepG2 Cell. Methods After HepG2 cell were treaded by ten repeated cycles of exposure at 43 degree C for 80 minutes twice a day，the sensibility of HepG2 cell to Adfiamyein was analyzed by MTr assay.The apoptosis Was detected by kit，and the expression of Bcl-2 or Bax protein and mRNA were detected by immunohistochemical method and RT-PCR respective.Results The drug resistance to Adfiamycin Was gained by HepG2 cell after multiple thermotherapy.The rate of apoptosis was decreased，the expression of Bcl一2 protein and mRNA Was strengthened，and the ratio of Bcl-2/Bax increased.Conclusions The resistance of heated HepG2 cell to chemotherapeutics Was related with the decreased rate of apoptosis，overexpression of Bcl-2 protein and mRNA，and increased ratio of Bcl-2/Bax.

Objective To investigate the expression change of ghtathione S-transferase π(GSTπ)protein and mRNA in the HepG2 cell after multiple thermotherapy.Methods HepG2 cells were treaded by ten repeated cycles of exposure at 43 degree C for 80 minutes twice a day，the sensibility of HepG2 cell to Adriamycin was analyzed by MTr assay，and the expression of QSTπprotein and mRNA were detected by immunohistochemical method and RT-PCR.Results The drug resistance to Adriamycin was gained by HepG2 cells after multiple thermotherapy，and the expression of GSTπ protein and mRNA wag strengthened.Conclusions The resistance of heated HepG2 cells to chemotherapeutics was concerned with overexpression of GSTπ protein and mRNA.

In recent years, the incidence of hyperlipidemic acute pancreatitis (HLAP) has gradually increased.HLAP is more dangerous than biliary and alcoholic acute pancreatitis. It develops rapidly, has many complications, and has a high mortality rate, which may be closely related to the etiology of HLAP. The causes of HLAP are complex and diverse, and there are many cases reported in the relevant literature. This article focuses on the primary causes (such as type Ⅰ, type Ⅳ and type V hyperlipidemia) and secondary causes (such as diabetes, pregnancy, drugs, obesity, etc), the article will summarize the research status of HLAP etiology at home and abroad.

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world,and its incidence is on the rise.Surgical resection is the standard method for the treatment of primary or metastatic HCC.In the past ten years,the local ablation of liver tumor has become more and more mature,and it has been proved to be an effective method for the treatment of malignant liver diseases.Whether used alone or in combination,it can control the growth of the tumor to a certain extent and prolong the survival time.It also improves the quality of life.This article begins with the mechanism of radiofrequency ablation in the treatment of liver cancer,and introduces in detail the research progress in the treatment of small liver cancer,large liver cancer,huge liver cancer and metastatic liver cancer by radio frequency ablation and the evaluation of the curative effect after operation.

Objective To investigate the effects of N-acetyl-D-glucosamine(GlcNAc)on acute pancreatitis in rats.Methods Twenty male SD rats were randomly divided into a control group,AP group,low GlcNAc + AP group and high GlcNAc + AP group,with five rats in each group.Acute pancreatitis was induced in AP group,low GlcNAc + AP group and high GlcNAc + AP group by two intraperitoneal injections of 2.5 g/kg L-arginine with a 1 hour interval.Among them,low GlcNAc + AP group and high GlcNAc + AP group were administered 50 and 200 mg/kg GlcNAc,respectively,by intraperitoneal injection at 24 hours before the first intraperitoneal injection of L-arginine.Group control and AP were intraperitoneally injected with the same volume of normal saline.After 24 h,the rats were sacrificed,and serum and pancreatic tissues were collected.Pancreatic tissue morphology was observed by HE staining,and serum levels of amylase(AMY),lipase(LPS),interleukin-1β(IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD)and malondialdehyde(MDA)were measured by enzyme-linked immunosorbent assay.Protein expression of nuclear factor E2-related factor 2(NRF2),heme oxygenase-1(HO-1),and peroxisome proliferator-activated receptor-γ(PPAR-γ)in pancreatic tissue was detected by Western Blot.Cluster of differentiation(CD)86,CD206 and macrophage markers(F4/80)were detected by immunofluorescence.Expression of CD86 and CD206 in pancreatic tissue was detected by immunohistochemistry.Results(1)Compared with control group,AMY,LPS,IL-1β,IL-6,TNF-α,and MDA levels and pancreatic CD86 expression in AP group were significantly increased(P<0.05),while SOD activity,protein expression levels of NRF2,HO-1,and PPAR-γ,and pancreatic CD206 expression were significantly decreased(P<0.05).(2)Compared with AP group,serum IL-1β,IL-6,TNF-α,MDA,and LPS and the pancreatic CD86 expression in low GlcNAc + AP group were significantly decreased(P<0.05).The PPAR-γ protein level in the pancreas was significantly increased(P<0.05).(3)Compared with AP group,serum AMY,LPS,IL-1β,IL-6,TNF-α,and MDA and pancreatic CD86 expression in high GlcNAc + AP group were significantly decreased(P<0.05),while serum SOD,and NRF2,HO-1,PPAR-γ,and pancreatic CD206 expression were significantly increased(P<0.05).(4)Compared with low GlcNAc + AP group,serum LPS,IL-1β and IL-6 in high GlcNAc + AP group were significantly decreased(P<0.05).Pancreatic expression of HO-1,PPAR-γ,and pancreatic CD206 were significantly increased(P<0.05).Conclusion GlcNAc treatment attenuates acute pancreatitis injury in AP rats,possibly by activating the NRF2/HO-1 signaling pathway to inhibit oxidative stress and promoting M2 macrophage polarization to attenuate pancreatic injury in AP rats.