title: The neuroprotective effect of modified "Shengyu" decoction is mediated through an anti-inflammatory mechanism in the rat after traumatic brain injury.
abstract: BACKGROUND
  "Shengyu" decoction, a traditional Chinese medicine, has been used to treat diseases with deficit in "qi" and "blood" induced frequently by profound loss of blood or by long sores with heavy pus, in which a potential anti-inflammatory effect is implied. The modified "Shengyu" decoction (MSD) used in the present study was designed on the basis of the "Shengyu" decoction, additional four herbs were added in. Many ingredients in these herbs have been demonstrated to be anti-inflammatory and thus MSD may be used for the treatment of traumatic brain injury (TBI). To evaluate the neuroprotective effect and the underlying mechanisms of MSD on the rat brain after TBI.
  
  
  METHODS
  TBI was induced in the right cerebral cortex of male adult rats using Feeney's weight-drop method. The rats were administered a gavage of MSD (0.5, 1.0 or 2.0 ml/200 g) 6h after TBI. The neurological functions, brain water content, contusion volume, and neuron loss were determined. The levels of TNF-α, IL-1β, IL-6, and IL-10 and the number of GFAP- and Iba1-positive cells in the brain ipsilateral to TBI were also measured. Moreover, the influence of MSD on these variables was observed at the same time.
  
  
  RESULTS
  The neurological deficits, brain water content, and neuron loss were significantly reduced after 1.0 or 2.0 ml/200 g of MSD treatment but not after 0.5 ml/200 g. In addition, treatment with MSD (1.0 ml/200 g) significantly increased the level of IL-10 and reduced the level of TNF-α and IL-1β and the number of GFAP- and Iba1-positive cells after TBI. However, the contusion volume of brain tissue and the expression of IL-6 were not significantly changed.
  
  
  CONCLUSIONS
  MSD may be a potential therapeutic for the treatment of TBI because MSD alleviated secondary brain injury induced by TBI. In addition, MSD inhibited the inflammatory response through reducing the expression of inflammatory cytokines and the activation of microglial cells and astrocytes in the brain tissue of rats after TBI. Therefore, a potential anti-inflammatory mechanism of the "Shengyu" decoction was confirmed, which may be one of the main reasons of "Shengyu" decoction used to treat diseases with obvious inflammatory responses.
authors.affiliation: Department of Neuropharmacology, Institute of Nautical Medicine, Nantong University, 19 Qixiu Road, Chongchuan District, Nantong, Jiangsu 226001, China; Department of Neurology, Affiliated Hospital, Nantong University, 20 Xishi Road, Chongchuan District, Nantong, Jiangsu 226001, China; Department of Neurology, The People's Hospital of Gaocheng, Hebei 052160, China.
authors.forename: Guang-Wei
authors.initials: GW
authors.lastname: Zhao
authors.affiliation: Department of Neurosurgery and Chinese Medicine, The People's Hospital of Nantong, Jiangsu 226001, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Neurosurgery, The People's Hospital of Ningxia, Yinchuan, Ningxia 750021, China. Electronic address: yclee7833@hotmail.com.
authors.forename: Yong-Cai
authors.initials: YC
authors.lastname: Li
authors.affiliation: Department of Neuropharmacology, Institute of Nautical Medicine, Nantong University, 19 Qixiu Road, Chongchuan District, Nantong, Jiangsu 226001, China; Department of Neurology, Affiliated Hospital, Nantong University, 20 Xishi Road, Chongchuan District, Nantong, Jiangsu 226001, China. Electronic address: jiangzl@ntu.edu.cn.
authors.forename: Zheng-Lin
authors.initials: ZL
authors.lastname: Jiang
authors.affiliation: Department of Neuropharmacology, Institute of Nautical Medicine, Nantong University, 19 Qixiu Road, Chongchuan District, Nantong, Jiangsu 226001, China.
authors.forename: Li
authors.initials: L
authors.lastname: Sun
authors.affiliation: Department of Neurosurgery and Chinese Medicine, The People's Hospital of Nantong, Jiangsu 226001, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Xi
authors.affiliation: Department of Neurosurgery, The People's Hospital of Ningxia, Yinchuan, Ningxia 750021, China.
authors.forename: Peng
authors.initials: P
authors.lastname: He
authors.affiliation: Department of Neuropharmacology, Institute of Nautical Medicine, Nantong University, 19 Qixiu Road, Chongchuan District, Nantong, Jiangsu 226001, China.
authors.forename: Guo-Hua
authors.initials: GH
authors.lastname: Wang
authors.affiliation: Department of Neurosurgery, The People's Hospital of Ningxia, Yinchuan, Ningxia 750021, China.
authors.forename: Shi-Hui
authors.initials: SH
authors.lastname: Xu
authors.affiliation: Department of Neurosurgery, The People's Hospital of Ningxia, Yinchuan, Ningxia 750021, China.
authors.forename: Dong-Ming
authors.initials: DM
authors.lastname: Ma
authors.affiliation: Department of Neurology, Affiliated Hospital, Nantong University, 20 Xishi Road, Chongchuan District, Nantong, Jiangsu 226001, China.
authors.forename: Kai-Fu
authors.initials: KF
authors.lastname: Ke
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001923:Brain Chemistry; D001930:Brain Injuries / Q000188:drug therapy*; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D008297:Male; D018696:Neuroprotective Agents; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014867:Water / Q000737:chemistry
chemical_list: D000893:Anti-Inflammatory Agents; D004365:Drugs, Chinese Herbal; D018696:Neuroprotective Agents; D014867:Water
keywords: AGE; GFAP; IL-10; IL-1β; IL-6; Iba1; Inflammatory response; LPS; MSD; Modified “Shengyu” decoction; Neuroprotection; No; PBS; RAGE; Rat; TBI; TNF-α; Traumatic brain injury; advanced glycation end product; glial fibrillary acidic protein; interleukin-10; interleukin-1β; interleukin-6; ionized calcium binding adapter molecule-1; lipopolysaccharide; modified “Shengyu” decoction; nitric oxide; phosphate-buffered saline; receptor for advanced glycation end product; traumatic brain injury.; tumor necrosis factor-α