Institute of Digestive Diseases, Department of Pathophysiology, Tongji University School of Medicine, 1239 Si Ping Road, Shanghai, 200092, China.
Cell Stress Chaperones. 2010 Nov;15(6):965-75. doi: 10.1007/s12192-010-0207-9. Epub 2010 Jun 24.
The objective of this study was to investigate the function of heat shock protein 60 (HSP60) on pancreatic tissues by applying HSP60 small interfering RNA (siRNA) to reduce HSP60 expression. Rat pancreas was isolated and pancreatic tissue snips were prepared, cultured, and stimulated with low and high concentrations of cerulein (10(-11) and 10(-5) mol/L) or lipopolysaccharide (LPS, 10 and 20 μg/mL). Before the stimulation and 1 and 4 h after the stimulation, the viability and the level of trypsinogen activation peptide (TAP) in the tissue fragments were determined and the levels of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) in the culture supernatants were measured. Real-time PCR and Western blotting were used to evaluate the HSP60 mRNA and protein expression. After the administration of siRNA to inhibit HSP60 expression in the isolated tissues, these injury parameters were measured and compared. The pancreatic tissues in the control (mock-interfering) group showed a decreased viability to varying degrees after being stimulated with cerulein or LPS, and the levels of TAP, TNF-α, and IL-6 increased significantly (p < 0.05) in the tissues and/or in the culture supernatant. The expressions of HSP60 mRNA and protein were raised moderately after stimulating 1 h with low concentrations of cerulein or LPS, but decreased with high concentrations of the toxicants. In particular, the expression of HSP60 protein was reduced significantly (p < 0.05) when the tissues were stimulated by the two toxicants for 4 h. In contrast, the tissue fragments in which HSP60 siRNA was applied showed much lower tissue viability (p < 0.01) and higher levels of TNF-a, IL-6, and TAP (p < 0.01) in the tissues or culture supernatant after stimulating with the toxicants at the same dose and for the same time duration as compared with those of the control groups (p < 0.05). The results indicated that both cerulein and LPS can induce injuries on isolated pancreatic tissues, but the induction effects are dependent on the duration of the stimulation and on the concentrations of the toxicants. HSP60 siRNA reduces HSP60 expression and worsens the cerulein- or LPS-induced injuries on isolated pancreatic tissues, suggesting that HSP60 has a protective effect on pancreatic tissues against these toxicants.
本研究旨在通过应用热休克蛋白 60(HSP60)小干扰 RNA(siRNA)降低 HSP60 表达来研究 HSP60 对胰腺组织的功能。分离大鼠胰腺并制备胰腺组织切片,培养并分别用低浓度(10^-11 和 10^-5 摩尔/升)和高浓度(10^-11 和 10^-5 摩尔/升)的 cerulein 或脂多糖(LPS,10 和 20 微克/毫升)刺激。在刺激前和刺激后 1 和 4 小时,测定组织片段的活力和胰蛋白酶原激活肽(TAP)水平,并测定培养上清液中肿瘤坏死因子-α(TNF-α)和白细胞介素 6(IL-6)的水平。采用实时 PCR 和 Western blot 评估 HSP60 mRNA 和蛋白表达。在分离组织中给予 siRNA 抑制 HSP60 表达后,测量这些损伤参数并进行比较。在对照(mock-interfering)组中,用 cerulein 或 LPS 刺激后,胰腺组织的活力不同程度降低,组织和/或培养上清液中 TAP、TNF-α和 IL-6 水平显著升高(p<0.05)。用低浓度 cerulein 或 LPS 刺激 1 小时后,HSP60 mRNA 和蛋白表达适度升高,但用高浓度毒物刺激时则降低。特别是,用两种毒物刺激 4 小时后,HSP60 蛋白表达明显降低(p<0.05)。相反,与对照组相比,在相同剂量和相同时间刺激毒物后,应用 HSP60 siRNA 的组织片段在组织或培养上清液中的组织活力(p<0.01)和 TNF-a、IL-6 和 TAP 水平(p<0.01)均明显更高(p<0.05)。结果表明,cerulein 和 LPS 均可诱导分离的胰腺组织损伤,但诱导作用取决于刺激持续时间和毒物浓度。HSP60 siRNA 降低 HSP60 表达并加重 cerulein 或 LPS 诱导的分离胰腺组织损伤,提示 HSP60 对胰腺组织具有保护作用,可抵抗这些毒物。