Objective To review the advancement of heat shock protein 70 (HSP70) vaccine in alimentary canal cancer. Methods Related articles were reviewed. Results HSP70 can integrate with tumor special antigen to form HSP70 polypeptide compound. To activate the special and nonspecial immune response of body, HSP70 can participate in the process of tumor immunity as a “molecular partner”. Conclusion HSP70 has shown alluring perspective in the precaution and treatment of alimentary canal cancer.
ObjectiveTo investigate the expression of heat shock proteins 90α(HSP90α) in human hepatocellular carcinoma and the relationship between its expression and biologic behavior of tumor and prognosis. MethodsUsing the immunohistochemical SP method, HSP90α expression was detected in liver tissue from 10 normal individuals, 40 patients with hepatocellular carcinoma(HCC) and adjacent noncancerous liver tissues. ResultsThe positive expression rate of HSP90α was 10.0%,52.5%,72.5% in normal liver tissues,adjacent noncancerous liver tissues,hepatocellular carcinous tissues respectively. A significantly higher distribution of HSP90α positive expression in HCC tissues compared with adjacent noncancerous liver tissues and normal liver tissues was obtained （P＜0.05）. The positive expression of HSP90α in HCC was correlated with clinical stage, tumor differentiation, serosal condition and lymph node metastasis （P＜0.05）, but not to tumor number （P＞0.05）. It was also correlated with prognosis of HCC. The mean tumorfree survival of patients with HSP90α negative expression was 38.6 months while that of HSP90α positive expression was 25.5 months （P＜0.05）. ConclusionHSP90α is overexpressed in human hepatocellular carcinoma. HSP90α could be used as an indicator to judge the clinical stage, tumor differentiation, serosal condition, lymph node metastasis and prognosis of HCC.
Objective To investigate the expressions of heat shock protein 27 (HSP27), Bcl-2, and Bax proteins of the nerve cells after spinal cord ischemia/reperfusion injury (SCII) in rats and their relationship. Methods Seventy adult male Sprague Dawley rats (weighing, 200-220 g) were randomly divided into the sham operated group (sham group, n=35) and the SCII group (n=35). Only the left renal artery was exposed with no occlusion of the abdominal aorta in the rats of sham group. The left renal artery was exposed with occlusion of the abdominal aorta for 20 minutes in the rats of SCII group. At 4, 8, and 12 hours and at 1, 2, 3, and 5 days, reperfusion treatment was performed in 5 rats respectively, and then the spinal cord tissue was harvested to detect the expressions of HSP27, Bcl-2, and Bax protein of the nerve cells by using immunohistochemistry staining. Results The HSP27 began to express at 4 hours, reached the peak at 3 days, and decreased at 5 days in SCII group; significant differences were found between at 3 and 5 days and at the other time points (P lt; 0.05). The Bcl-2 expression increased at 4 hours, reached the peak at 1 day and maintained a high level at 2 days, and then gradually decreased; significant differences were found between at 1 and 2 days and at the other time points (P lt; 0.05). The Bax expression reached the peak at 12 hours and 3 days, and decreased at 5 days; significant differences were found between at 12 hours and 3 days and at the other time points (P lt; 0.05). A little expression of each protein was observed in sham group at different time points; the expressions of HSP27, Bcl-2, and Bax proteins in SCII group were significantly higher than those in sham group at different time points (P lt; 0.05). Conclusion There may be the time window of self repair after SCII. High expression of HSP27 has an obvious protective effect on the SCII in rat, by promoting the expression of the anti-apoptotic protein Bcl-2 and reducing the expression of the pro-apoptotic protein Bax so as to inhibit spinal cord cell apoptosis.
Objective To investigate the role and mechanism of heat shock protein 60 (HSP60) in induction of murine skin allograft tolerance. Methods At the age of 8-12 weeks, inbred female BALB/C (H-2d) mice (n=45) and CBA/N (H-2k)mice (n=15) were used as transplantation donors and C57BL/6 (H-2b) mice (n=60) as recipients. Recipients C57BL/6 (H-2b) mice were randomized into 4 groups (n=15). In group A, 1 cm × 1 cm Wolfe-Krause skin graft was excised from the back of BALB/C (H-2d) mice and hypoderma was scraped off aseptically, and then transplanted to the back of C57BL/6 (H-2b)mice. The method of skin transplantation in the other 3 groups was the same as to group A. In group B, C57BL/6 (H-2b) mice were treated with imcompleted Freund’s adjuvant (IFA) administration into the back 2 weeks before transplantation of BALB/C (H-2d) mice skin. In group C, C57BL/6 (H-2b) mice were administered HSP60 emulsified in IFA into the back 2 weeks before transplantation of BALB/C (H-2d) mice skin. In group D, C57BL/6 (H-2b) mice were treated with HSP60 emulsified in IFA into the back and followed by skin transplantation of CBA/N (H-2k) mice 2 weeks later. The delayed type hypersensitivity was determined 7 days after transplantation. One-way mixed lymphocyte reaction, the concentration of cytokines in the mixed lymphocyte reaction culture supernatant was determined 7 days and 25 days after transplantation. The survival time of skin allograft was observed. Results The survival time of skin allograft in groups A, B, C and D was 12.4 ± 0.5, 11.6 ± 0.8, 29.3 ± 2.6 and 27.6 ± 2.1 days, respectively. There was significant difference between groups A, B and groups C, D (P﹤0.05), while there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). The counts of per minute impulse (cpm) of mixed lymphocyte reaction 7 days after transplantation in groups A, B, C and D was 12 836 ± 1 357, 11 876 ±1 265, 6 581 ± 573 and 6 843 ± 612, respectively. There was significant difference between groups A, B and group C and group D (P lt; 0.05), while there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). The cpm of mixed lymphocyte reaction at 25 days after transplantation in group A, B, C and D was 13 286 ±1 498, 12 960 ± 1 376, 11 936 ± 1 265 and 12 374 ± 1269, respectively. There was no significant difference among 4 groups (P gt;0.05).The concentration of IL-10 in the mixed lymphocyte reaction culture supernatant in groups C, D were higher than that in groups A, B, and IL-2 and IFN-γ were lower than that in groups A, B 7 days after transplantation (P lt; 0.05), while there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). There was no significant difference in cytokines among the 4 groups 25 days after transplantation (P gt; 0.05). The delayed type hypersensitivity in groups A, B, C and D 7 days after transplantation was 0.84 ± 0.09, 0.81 ± 0.07, 0.43 ± 0.05 and 0.46 ± 0.03 mm, respectively. There was significant differences between groups A, B and groups C, D (P lt; 0.05). While there was no significant difference between group A and group B as well as between group C and group D (P gt; 0.05). Conclusion HSP60 may play a role in induction and maintenance of murine skin allograft tolerance.
Objective To study the expression of heat shock protein 47 (HSP47) and its correlation to collagen deposition in pathological scar tissues. Methods The tissues of normal skin(10 cases), hypertrophic scar(19 cases), and keloid(16 cases) were obtained. The expression ofHSP47 was detected by immunohistochemistry method. The collagen fiber content was detected by Sirius red staining and polarization microscopy method. Results Compared with normal skin tissues(Mean IOD 13 050.17±4 789.41), the expression of HSP47 in hypertrophic scar(Mean IOD -521 159.50±272994.13) and keloid tissues(Mean IOD 407 440.30±295 780.63) was significantly high(Plt;0.01). And there was a direct correlation between the expression of HSP47 and the total collagen fiber content（r＝0.386，Plt;0.05）. Conclusion The HSP47 is highly expressed in pathological scartissues and it may play an important role in the collagen deposition of pathological scar tissues.
Objective To detect the expression of heat shock protein 47 mRNA in pathological scar tissue by using real-time fluorescent quantitative reversetranscription-polymerase chain reaction (RT-PCR). Methods The tissues of normal skin(n=6), hypertrophic scar(n=6) and keloid(n=6) were adopted, which were diagnosised by Pathology Department. Based on fluorescent TaqMan methodology, the real-time fluorescent quantitative RT-PCR were adopted to detect the expression ofheat shock protein 47 mRNA. Results Compared with normal skin tissue（0.019±0.021）×105, the expressions of heat shock protein47 cDNA of hypertrophic scar tissue（1.233±1.039）×105 and keloid tissue（1.222±0.707）×105 were higher， being significant differences（Plt;0.05）. Conclusion A fluorescent quantitative method was successfully applied to detecting the expression of heat shock protein 47 mRNA. Heat shock protein 47 may play an important role in promoting the formation of pathological scar tissue.
Objective To observe the expression of heat shock protein 70 (HSP70) in human liver after hepatic transplantation, and to study its correlation with the occurrence and progression of acute allograft rejection.Methods Fifteen biopsy specimen of allograft liver after transplantation were collected and divided into three groups according to their pathological changes: control group (no rejection), mild acute rejection group, and moderate/serious acute rejection group. The expressions of HSP70 in grafts were detected by using immunohistochemical method and imaging analysis. Results HSP70 was expressed in all 3 groups, and appeared mainly in hepatocellular cytoplasm. The immunohistochemical imaging analysis of HSP70 showed: integral optical density (IOD) which was 30.99±11.14 in the control group was lower than that in the mild acute rejection group (68.84±21.37) and that in the moderate/serious acute rejection group (71.82±19.99), P＜0.01； and the IOD in the moderate/serious acute rejection group was higher than that in the mild acute rejection group (P＜0.05). Conclusion HSP70 plays a role in cellular protection for allograft liver, and the continuously increasing expression of HSP70 in graft maybe closely relates to the occurrence and progression of acute allograft rejection.
Objective To study the effects of heat shock proteins (HSPs) in the course of hepatic ischemia reperfusion injury (HIRI), and analyze its mechanism. Methods The relationship between HSPs and HIRI was studied by reviewing literatures. Results HSPs was a kind of stress protein induced after cell was sitmulated by the stress. It could improve body′s tolerance to tough situation. Though hepatic ischemia reperfusion usually results in serious hepatic injury, at the same time it could induce can increase the production of HSPs that can protect liver from and lessen ischemia reperfusion injury. Conclusion HSPs can improve the tolerance to HIRI and lessen injury. In addition, HSPs is thought to be markers of HIRI, and can be used as a efficient indicator to test the level of hepatic injury and assess prognosis.
ObjectiveTo investigate the inhibitory effect of heat shock protein 90 (HSP90) inhibitors of 17-propylene amino-17-demethoxy geldanamycin (17-AAG) combining with paclitaxel on human anaplastic thyroid cancer FRO cell line. Method①The proliferation inhibition rates of FRO cells were detected by mmethyl thiazolyl tetrazolium (MTT) assay in different concentration groups (17-AAG: 0.312 5, 0.625 0, 1.2500, 2.5000, and 5.0000 μmol/L; paclitaxel: 0.001 0, 0.0100, 0.1000, and 1.0000 μmol/L; combination group, 17-AAG: 0.625 0 μmol/L, paclitaxel: 0.001 0, 0.0100, 0.1000, and 1.0000 μmol/L) and at different time points (24, 48, and 72 hours). ②The change of cell cycle and apoptosis rates of FRO cells were detected in 17-AAG group (0.625 0 μmol/L), paclitaxel group (0.1000 μmol/L), and combination group (17-AAG: 0.625 0 μmol/L, paclitaxel: 0.1000 μmol/L) by flow cytometry at 24 hours after treatment. ③activity of Caspase-3 and Caspase-9 in FRO cells of 17-AAG group (0.625 0 μmol/L), paclitaxel group (0.1000 μmol/L), and combination group (17-AAG: 0.625 0 μmol/L, paclitaxel: 0.1000 μmol/L) was detected by Caspase-3 detection reagent box and Caspase-9 detection reagent box respectively. FRO cells of normal control group were treated without any drug, but culture solution. Results①The proliferation inhibition rates of FRO cells increased with the increase of concentra-tion (17-AAG, paclitaxel, combination of 17-AAG and paclitaxel), there was significant difference between any 2 groups (normal control group included), P<0.05. In addition, the proliferation inhibition rates of FRO cells in any concentration group (normal control group excluded) increased over time (24, 48, and 72 hours), there was significant difference between any 2 time points (P<0.05). The proliferation inhibition rates of FRO cells in combination group were all higher than those of 17-AAG group and paclitaxel group in condition of same time point and same concentration (P<0.05). The q value of combination group was higher than 1.15 at 3 time points in all concentration, that meant 17-AAG could increase the efficiency of paclitaxel. ②The apoptosis rate of FRO cells in normal control group was lower than those of 17-AAG group, paclitaxel group, and combination group (P<0.05), and apoptosis rate of FRO cells in combination group was higher than those of 17-AAG group and paclitaxel group (P<0.05). ③Activity of Caspase-3 and Caspase-9 of FRO cells in normal control group were lower than those of 17-AAG group, paclitaxel group, and combination group (P<0.05), and activity of Caspase-3 and Caspase-9 of FRO cells in combination group were higher than those of 17-AAG group and paclitaxel group (P<0.05). Conclusions17-AAG and paclitaxel can significantly inhibit the proliferation and induce the apoptosis of FRO cells. The combination of the two kinds of drugs may generate synergy, with dose-dependence effect.
Objective To explore the effect of epidural analgesia for labor on maternal temperature and the newborns. Methods This randomized trial was performed in West China Second Hospital between December 2015 and July 2016. Fifty puerperants were randomly divided into epidural analgesia (EA) group (natural labor under EA, n=25) or the control group (natural labor using Ramaze breathing method, n=25). Maternal tympanic temperature was recorded once per hour after treating with painless labor or blank control. The serum interleukin-1 beta (IL-1β) and heat shock protein 70 (HSP70) level were measured from the blood of the umbilical cord after the delivery. Apgar scores of the newborns were also recorded. Results There was a significant difference in the temperature between EA and control group one hour after the treatment of painless labor [ (36.9±0.7) and (36.4±0.5)℃]. The level of serum IL-1β and HSP70 were significantly higher in EA group [IL-1β: (0.308±0.036) ng/mL; HSP70: 1.175±0.196] than those in the control group [IL-1β: (0.244±0.031) ng/mL; HSP70: 0.935±0.308] (P<0.05). However, no significant difference was found in the neonatal Apgar score (P>0.05). Conclusions The increase of maternal temperature is greater in the EA labor puerperants compared with that in the controls, which may be related to the increase of IL-1β and HSP70. No adverse effect of labor analgesia on new borns is found