Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis

Forty Wistar rats were divided into 5 groups, including the control group, the acute pancreatitis group (AP group, induced by intraperitoneal injections of caerulein), and the AP group treated with baicalin, the AP group treated with LPS, and the AP group treated with LPS and baicalin. Pathological...

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Main Authors: Dongbo Xue, Weihui Zhang, Yingmei Zhang, Haiyang Wang, Biao Zheng, Xingye Shi
Format: Article
Language:English
Published: Wiley 2006-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/MI/2006/26295
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author Dongbo Xue
Weihui Zhang
Yingmei Zhang
Haiyang Wang
Biao Zheng
Xingye Shi
author_facet Dongbo Xue
Weihui Zhang
Yingmei Zhang
Haiyang Wang
Biao Zheng
Xingye Shi
author_sort Dongbo Xue
collection DOAJ
description Forty Wistar rats were divided into 5 groups, including the control group, the acute pancreatitis group (AP group, induced by intraperitoneal injections of caerulein), and the AP group treated with baicalin, the AP group treated with LPS, and the AP group treated with LPS and baicalin. Pathological damage of pancreatic tissue was scored with hematoxylin and eosin (HE) staining. The mRNA expression of TNF-α was measured with semiquantitative RT-PCR, and activation of NF-κB was detected with flow cytometry assay. It was shown in the results that the expression of TNF-α mRNA, activation of NF-κB, and pathological score of AP group were all obviously higher than those of control group (P<.01). In AP group treated with LPS, further rise of these values were observed (P<.01). In the AP group treated with baicalin, activation of NF-κB decreased (P<.05), and expression of TNF-α mRNA also obviously decreased (P<.01), while pancreatic pathological damage was alleviated at the same time (P<.01); similar results were observed in AP group treated with LPS and baicalin (P<.01), which indicated that baicalin might be applied to inhibit NF-κB activating and TNF-α expressing so as to treat AP.
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institution Kabale University
issn 0962-9351
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publishDate 2006-01-01
publisher Wiley
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series Mediators of Inflammation
spelling doaj-art-fe4860990c264afb958de23d5197f59e2025-02-03T01:02:05ZengWileyMediators of Inflammation0962-93511466-18612006-01-01200610.1155/MI/2006/2629526295Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute PancreatitisDongbo Xue0Weihui Zhang1Yingmei Zhang2Haiyang Wang3Biao Zheng4Xingye Shi5Department of General Surgery, First Clinical College, Harbin Medical University, Harbin 150001, ChinaDepartment of General Surgery, First Clinical College, Harbin Medical University, Harbin 150001, ChinaCentral Laboratory, First Clinical College, Harbin Medical University, Harbin 150001, ChinaDepartment of General Surgery, First Clinical College, Harbin Medical University, Harbin 150001, ChinaDepartment of General Surgery, First Clinical College, Harbin Medical University, Harbin 150001, ChinaDepartment of General Surgery, First Clinical College, Harbin Medical University, Harbin 150001, ChinaForty Wistar rats were divided into 5 groups, including the control group, the acute pancreatitis group (AP group, induced by intraperitoneal injections of caerulein), and the AP group treated with baicalin, the AP group treated with LPS, and the AP group treated with LPS and baicalin. Pathological damage of pancreatic tissue was scored with hematoxylin and eosin (HE) staining. The mRNA expression of TNF-α was measured with semiquantitative RT-PCR, and activation of NF-κB was detected with flow cytometry assay. It was shown in the results that the expression of TNF-α mRNA, activation of NF-κB, and pathological score of AP group were all obviously higher than those of control group (P<.01). In AP group treated with LPS, further rise of these values were observed (P<.01). In the AP group treated with baicalin, activation of NF-κB decreased (P<.05), and expression of TNF-α mRNA also obviously decreased (P<.01), while pancreatic pathological damage was alleviated at the same time (P<.01); similar results were observed in AP group treated with LPS and baicalin (P<.01), which indicated that baicalin might be applied to inhibit NF-κB activating and TNF-α expressing so as to treat AP.http://dx.doi.org/10.1155/MI/2006/26295
spellingShingle Dongbo Xue
Weihui Zhang
Yingmei Zhang
Haiyang Wang
Biao Zheng
Xingye Shi
Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis
Mediators of Inflammation
title Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis
title_full Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis
title_fullStr Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis
title_full_unstemmed Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis
title_short Adjusting Effects of Baicalin for Nuclear Factor-κB and Tumor Necrosis Factor-α on Rats With Caerulein-Induced Acute Pancreatitis
title_sort adjusting effects of baicalin for nuclear factor κb and tumor necrosis factor α on rats with caerulein induced acute pancreatitis
url http://dx.doi.org/10.1155/MI/2006/26295
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