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1、 WU Hong, et al. The Second Affiliated Hospital of Hunan Medical University, Changsha 410011, Hunan Province, China 179 and the activity of IL1 produced by monocyte after treatment decreased compared with that before treatment (P 0. 01, Figure 5). In the control group, the plasma FN, FNR and TNFa an
2、d the activity of IL-1 had no significant changes (P0. 05, Figures 2 5) after treatment with routine methods. Qinicol profilesIn 63. 5 % patients with cirrhotic HBV, serum globulin amount was down-regulated to norml levels after treatment with YGJY decoction, but only in 23. 4% patients treated by r
3、outine methods. DISCUSSION Recent researches in cirrhosis have focused on interaction between the cytokine and extracellular matrix (ECM) h 8,9 . Several reports have shown that serum levels of some ECM molecules, such as type Illprocolla- gen peptide, types I and IV collagen and fibronectin, were g
4、ood markers of hepatic fibrosis and ECM accumulation played a major role in the liver function impairment. The FN and FNR are the main component of extracellular matrix. We found that in patients in decom- pencated stage of liver cirrhosis, the plasma FN was significantly lower and FNR was significa
5、ntly higher, with a strong negative correlation (r = 0. 6534). The TNF and IL-1 activity were also increased as compared with the normal subjects (P0. 05). Toshiyuki Hagiwata101 et al have observed that recombinant human IL-1 could increase FN in the liver of rats and also could directly increase th
6、e transcription of type I, Illand IVcollagen1101 . IL-1 may act synergically with TNF-ct in inducing hepati- tis9. TNF-ct is a multifunctional cytokine which is thought to be able to regulate inflammatory and pathological processes and orchestrate necrosis regenerations. Recently, it has been shown
7、that TNFa can regulate liver cell regeneration positively11. These data show that serum FNR, IL-1 and TNF-a can up-regulate and FN can down regulate the liver fibrosis process. We found that IL-1 and FNR, reflecting the increased fibrosis in the liver, were strongly down-regulated by treatment with
8、YGJY decoction. In cirrhotic patients, FNR and activity of IL-1 significantly decreased after treatment as compared with that before treatment (PC0. 05); while FN, inhibiting liver fibrosis, was strongly up-regulated by YGJY decoction, and FN significantly increased as compared with that before the
9、treatment (P0. 01). These changes showed that YGJY decoction can prevent liver damage and inhibit the hepatic fibrosis. After treatment with YGJY decoction, TNFa was elevated in the cirrhotic patients. We detected plasma level of TNFa and nirate in cirrhotic rats by reproduction with CCL4 and found
10、that the TNFa was significantly higher after treatment than before treatment. It has been shown that TNF-a can positively regulate the hepa- tocyte proliferation in rats induced by the nitratetll. Further studies are necessary to clarify the effect and mechanism of YGJY decoction in the hepatocyte p
11、roliferation and regeneration. REFERENCES 1 Yamaucihi M, Nakajima H, Ohata M, Hirakawa J, Mieuilara Y, Nakahara M, et fl/. Detection of fibronectin receptor in sera: Its clinical significance as a parameter of hepatie fibrosiss. Hepatology-, 1991; 14(2): 244-250 2 Gabrielli GB, Casaril M, Bonazzil B
12、aracchino F, Bellisola G, Corrocher R. Plasma fibronectin in liver cirrhosis and its diagnostic value. Clinica Chimica Acta-, 1986; 160 (3): 289-296 3 Matsuoka M, Plam NT, Taukamoto M. Differential effects of interleukin-1, tumor necrosis factor and transforming growth factor betal on cell prolifera
13、tion and collagen formation by cultured fat-storing cells. Liver, 1989; 9 (9): 71-78 4 Wu H, Wang ZM, Fan JT, Deng JW, Fen TJ. Effect of six kinds of dcoctions on experimental autoimmune liver diseases. Bulletin Human Med Univ, 1991; 16 (3): 263-267 5 Qien JZ, Li ZM. Internal medicine. Ed 3. Beijing
14、: The People s Medical Publishing House, 1989:389-396 6 Habicht GS, Beck G, Benach JL, James L, Colemanand Leichting KD. Lyme disease spirochetes induce human and murine interleukin-1 production. J Immunol-, 1985; 134(5):3147-3154 7 Pizzaro TT, Malinowskak K, Kovacs EJ, Chancy J, Bobinson JA, Piclin
15、ini LA. Induction of TNFa and FNF(3 (Lymphotoxin) gene expression during rate Cardige gllogr of regection (Abstract). FASEB J, 1991; 5 (A): 1708 8 Dinaretto CA. Interleukin-1 and Interleukin antagonism blood., 1991; 77 (8): 1627-1862 9 Gantner F, Leist M, Lohes AW, Germaann RG, Tes G. Concaavalin Ai
16、nduced T cell-mediated hepatic inujury in mice: the role of Tumor necrosis factor. Hepatology, 1995;2(1): 190-198 10 Hagiwata T, Suzuid H, Kano G Kashiwag I, Ykyama Y, Onoiaki K. Regulation of fibronectin synthesis by inteleukin-1 and interleukin-6 in rat hepatocytes. Am J Pathol, 1990; 136(1 ): 39-
17、47 11 Kubo Y, Yasenaga M, Masuha M, Terai S, Nakamura T, Okita K. Hepatocyte proliferation induced in rats by lead nitrate is suppressed by several tumor necrosis factors and inhibitors. Hepatology, 1996; 23(1): 104-114 ISSN 1006-9100 CN14-1212/R China Natl J New Gastroenterol, 1997; 3(3): 179 Effec
18、ts of electro-acupuncture on 5-HT, NOS and gastric mucosa in stress rats ZHU Shun-Li, XU Guan-Sun, WANG ZhervJiu, CHEN Quan-Zhu and JIAO Jie Institute of Acupuncture and Meridians, Anhui College of Traditional Chinese Medicine, Hefei 230038, Anhui Province, China Subject headings electroacupuncture
19、; serotonin/acu-moxibustion effects? aminoacid oxidoreduc- tases/acu moxibustion effects; gastric mucosa/acu moxibustion effects Abstract AIM To study the effects of electro-acupuncture (EA) on 5-hn, NOS, NO and gastric mucosa in stress rats. METHODS By biochemical methods, the changes of 5-hn and N
20、OS in gastric mucosa NO and 5-hn in serum were anaHysed and the gastric mucosa was examined pathohistologically in stress rats with gastric mucosa damage after EA. The changes before and after stress by EA were compared. RESULTS EA decreased gastric mucosa damage index in the stress rats (2. 71 0. 4
21、0 to 1. 86 +0. 69, P 0. 01). EA tDrmalized NOS level in gastric mucosa to the control group. The changes before stress by EA was more obvious than the EA after stress; EA low- ered the 5-KT contents of gastric mucosa Og/g wet weight, 6. 91 3. 08 to 4. 51 1. 62, P 0. 01). EA recovered the NO level in serum of the stress rats Omol/L,5. 78 1. 49 to 7. 91 1. 11, P 0 05 ), and increased the contents of 5-KT and 5-HIAA in serum continuously. CONCLUSION EA stimulation normalizes the NOS and NO levels in gastric mucosa in stress rats, lowers the high 5-KT contents and induces NO releases.
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