清胰片治疗胰腺癌癌前病变实验研究
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摘要
目的:研究清胰片对大鼠胰腺癌癌前病变的影响。方法:将大鼠36只随机分为两组,即给药组、模型组,DMBA诱导大鼠建立胰腺炎模型,给药组清胰片连续灌胃半月,在术后2个月、4个月、6个月、9个月每组各处死大鼠4只, HE染色后,光镜下观察两组大鼠的病理改变情况。结果:两组术后尿淀粉酶显著升高,与术前比较具有统计学差异;在造模后2月,两组大鼠均以胰腺炎症为主要病理改变,以胰管周围纤维化、小叶结构紊乱、炎性渗出为主要表现,且由急性炎症转为慢性炎症;术后4个月两组均出现不同程度的轻中度不典型增生;术后9个月,给药组病理观察无恶变趋势;而对照组出现了重度不典型增生、低级别、高级别内瘤变(原位癌)。结论:胰腺炎与早期胰腺癌的发生存在高度相关性,7, 12-二甲基苯并蒽作为诱导剂可以诱导胰腺炎的发生,并向胰腺癌方向转化,清胰汤能逆转胰腺炎向胰腺癌的发生,有必要进一步研究其有效成分预防其恶性转化的分子生物学机制,为清胰片安全有效地应用于肿瘤早期病变奠定基础。
Objective: To research the effect of Qingyi tablets to precancerous lesion of pancreatic cancer. Methods:Rats were randomly divided into two groups: treatment group and control group.The model of pancreatitis was established by DMBA-induced rat. The treatment group was given Qingyi tablets by continuous intragastric administration for half a month. And in 2,4,6 and 9 months after operation,4 rats were respectively sacrificed in each group. After HE staining,the pathological changes of rats in two groups were observed under light microscope.Results: The level of urinary amylase became significantly higher in two groups after operation, which was statistically different from preoperation. In 2 months after modelling,the pancreatic inflammation of rats in both groups was main pathological change which showed mainly as the fibrosis around pancreatic duct,structural disorder of lobules and exudative inflammation as well as transition from acute inflammation to chronic inflammation. In 4 months after operation,mild or moderate atypical hyperplasia of different degrees occurred in both groups.In the observation for 9 months after operation,the pathology of treatment group had no malignant trend,while severe atypical hyperplasia,low and high grade neoplasia(carcinoma in situ)occurred in control group. Conclusion:Pancreatitis is highly correlated with the occurrence of early pancreatic cancer. 7,12-dimethyl benzanthracene,acting as an inducer,can induce the occurrence of pancreatitis which can transform to pancreatic cancer. Qingyi tablets can reverse the occurrence from pancreatitis to pancreatic cancer. It is necessary to further study the molecular biological mechanism of its active ingredients preventing the malignant transformation,in order to lay the foundation for the safe and effective clinical application of Qingyi tablets to early tumor lesion.
Objective: To research the effect of Qingyi tablets to precancerous lesion of pancreatic cancer. Methods:Rats were randomly divided into two groups: treatment group and control group.The model of pancreatitis was established by DMBA-induced rat. The treatment group was given Qingyi tablets by continuous intragastric administration for half a month. And in 2,4,6 and 9 months after operation,4 rats were respectively sacrificed in each group. After HE staining,the pathological changes of rats in two groups were observed under light microscope.Results: The level of urinary amylase became significantly higher in two groups after operation, which was statistically different from preoperation. In 2 months after modelling,the pancreatic inflammation of rats in both groups was main pathological change which showed mainly as the fibrosis around pancreatic duct,structural disorder of lobules and exudative inflammation as well as transition from acute inflammation to chronic inflammation. In 4 months after operation,mild or moderate atypical hyperplasia of different degrees occurred in both groups.In the observation for 9 months after operation,the pathology of treatment group had no malignant trend,while severe atypical hyperplasia,low and high grade neoplasia(carcinoma in situ)occurred in control group. Conclusion:Pancreatitis is highly correlated with the occurrence of early pancreatic cancer. 7,12-dimethyl benzanthracene,acting as an inducer,can induce the occurrence of pancreatitis which can transform to pancreatic cancer. Qingyi tablets can reverse the occurrence from pancreatitis to pancreatic cancer. It is necessary to further study the molecular biological mechanism of its active ingredients preventing the malignant transformation,in order to lay the foundation for the safe and effective clinical application of Qingyi tablets to early tumor lesion.
引文
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[5]郑建明,朱明华.胰腺上皮内瘤变[J].胰腺病学, 2004,4(2):116-120.
[6]杨小霞,郭庆捷,曹泽伟,等.清胰片治疗轻型急性胰腺炎38例临床观察[J].中医杂志,2014,55(13):1 127-1 129.
[7]RiveraCA, Wheeler MD, Enomoto N, et al.A rat model of pancreatic ductal adenocarcinoma:targeting chemical carcinogens[J]. Surgery, 1997,122(1):82-90.
[8]Z’graggen K, Warshaw AL, Werner J, et al.Promoting effect of a high-fat/high-protein diet in DMBA-induced ductal pancreatic cancer in rats[J]. Annals of surgery, 2001,233(5):688.
[9]DiteP,HermanovdM,TrnaJ,etal.Theroleofchronic inflammation:chronic pancreatitis as a risk factor of pancreatic cancer[J].Dig Dis,2012(30):277-283.
[10]Duell EJ,Lucenteforte E,Olson SH,et al.Pancreatitis and pancreatic cancer risk:a pooled analysis in the International Pancreatic Cancer Case Control Consortium[J].Ann Oncol,2012(23):2 964-2 970.
[11]Wang W,Liao Z,Li G,et a1.Incidence of pancreatic cancer in Chinese patients with chronic pancreatitis[J].Pancreatology,2011(11):1 623.
[12]Delgiomo,KE,Hall JC,Takeuchi kk,et al. Ke. Identification an d manipulation of biliary metaplasia in pancreatic tumors[J].Gastroenterology,2014,146(1):233-244.
[13]GuptaRK,hosroshahiA,ShinagareS,etal.Doesauto immune pancreatitis increase the risk of pancreatic carcinoma a retrospective analysis of pancreatic resections[J]. Pancreas.2013,42(3):506-510.
[2]Korc M. Pancreatic cancer-associated stroma production[J]. Am J Surg, 2007, 194(4 Suppl):S84-86.
[3]Andea A F, Sarkar. VN, Adsay, Clinicopathological correlates of pancreatic intraepithelial neoplasia:a comparative analysis of 82cases with and 152 cases without pancreatic ductal adenocarcinoma[J]. Modern pathology, 2003, 16(10):996-1 006.
[4]Konstantinidis IT,Vinuela EF,Tang LH, et al., Incidentally discovered pancreatic intraepithelial neoplasia:what is its clinical significance?[J]Annals of surgical oncology, 2013,20(11):3643-3 647.
[5]郑建明,朱明华.胰腺上皮内瘤变[J].胰腺病学, 2004,4(2):116-120.
[6]杨小霞,郭庆捷,曹泽伟,等.清胰片治疗轻型急性胰腺炎38例临床观察[J].中医杂志,2014,55(13):1 127-1 129.
[7]RiveraCA, Wheeler MD, Enomoto N, et al.A rat model of pancreatic ductal adenocarcinoma:targeting chemical carcinogens[J]. Surgery, 1997,122(1):82-90.
[8]Z’graggen K, Warshaw AL, Werner J, et al.Promoting effect of a high-fat/high-protein diet in DMBA-induced ductal pancreatic cancer in rats[J]. Annals of surgery, 2001,233(5):688.
[9]DiteP,HermanovdM,TrnaJ,etal.Theroleofchronic inflammation:chronic pancreatitis as a risk factor of pancreatic cancer[J].Dig Dis,2012(30):277-283.
[10]Duell EJ,Lucenteforte E,Olson SH,et al.Pancreatitis and pancreatic cancer risk:a pooled analysis in the International Pancreatic Cancer Case Control Consortium[J].Ann Oncol,2012(23):2 964-2 970.
[11]Wang W,Liao Z,Li G,et a1.Incidence of pancreatic cancer in Chinese patients with chronic pancreatitis[J].Pancreatology,2011(11):1 623.
[12]Delgiomo,KE,Hall JC,Takeuchi kk,et al. Ke. Identification an d manipulation of biliary metaplasia in pancreatic tumors[J].Gastroenterology,2014,146(1):233-244.
[13]GuptaRK,hosroshahiA,ShinagareS,etal.Doesauto immune pancreatitis increase the risk of pancreatic carcinoma a retrospective analysis of pancreatic resections[J]. Pancreas.2013,42(3):506-510.