title: Sinisan, a traditional Chinese medicine, attenuates experimental chronic pancreatitis induced by trinitrobenzene sulfonic acid in rats.
abstract: OBJECTIVE
  Sinisan, a traditional Chinese medicine, is effective for the treatment of gastrointestinal disorders. In this study, we investigated the potential protective role of Sinisan against chronic pancreatitis (CP) in rats.
  
  
  METHODS
  CP was induced in rats by intrapancreatic injection of trinitrobenzene sulfonic acid (TNBS). Rats were randomly divided into a sham group, a TNBS-induced CP group and a Sinisan-treated group. Serum amylase and histological score were used to evaluate the severity of disease. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), interleukin-10 (IL-10) and α-smooth muscle actin (α-SMA) were also measured in the three groups. Mechanical allodynia was measured with von Frey filaments. In addition, the protein levels of nerve growth factor (NGF) were measured in pancreatic tissues.
  
  
  RESULTS
  Administration of Sinisan significantly decreased the severity of CP. In the Sinisan-treated group, serum amylase, TNF-α, IL-1β, COX-2 and α-SMA levels were lower and the level of IL-10 was upregulated compared with the TNBS-induced CP group. Furthermore, treatment with Sinisan significantly, though not completely, attenuated the allodynia. Simultaneously NGF expression was also significantly downregulated in the Sinisan-treated group compared with the TNBS-induced CP group.
  
  
  CONCLUSIONS
  Sinisan could be an effective treatment modality for CP via its anti-inflammatory, anti-fibrotic and analgesic properties. It may be a promising drug candidate for the treatment of patients with CP.
authors.affiliation: Department of Medical Image Center, Chinese PLA 302 Hospital, Beijing, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Tang
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Liao
authors.forename: Nobuko
authors.initials: N
authors.lastname: Kawaguchi-Sakita
authors.forename: Vikram
authors.initials: V
authors.lastname: Raut
authors.forename: Elham
authors.initials: E
authors.lastname: Fakhrejahani
authors.forename: Niansong
authors.initials: N
authors.lastname: Qian
authors.forename: Masakazu
authors.initials: M
authors.lastname: Toi
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D016753:Interleukin-10 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D050500:Pancreatitis, Chronic / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016896:Treatment Outcome; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000199:Actins; D015415:Biomarkers; D051546:Cyclooxygenase 2; D004365:Drugs, Chinese Herbal; D016753:Interleukin-10; D053583:Interleukin-1beta; D014302:Trinitrobenzenesulfonic Acid; D014409:Tumor Necrosis Factor-alpha; C498862:Acta2 protein, rat