<p>Effects of transection of cervical sympathetic trunk on cognitive function of traumatic brain injury rats</p>

Abstract

Objective: To observe the effects of transection of cervical sympathetic trunk (TCST) on the cognitive function of traumatic brain injury (TBI) rats and the potential mechanisms. Methods: A total of 288 adult male SD rats were divided into 3 groups using a random number table: TBI group (n=96), TBI + TCST group (n=96) and Sham group (n=96). The water maze test was performed before TBI (T0) and at day 1 (T 1 ), day 2 (T 2 ), day 3 (T 3 ), 1 week (T 4 ), 2 weeks (T 5 ), 6 weeks (T 6 ) and 12 weeks (T 7 ) after TBI. The levels of α1-adrenergic receptors (α1-ARs), α2-adrenergic receptors (α2-ARs), toll-like receptor 4 (TLR-4) and P38 in hippocampi were detected by real-time PCR. Hippocampal P38 expression was assayed by Western blot. The expressions of interleukin-6 (IL-6), tumor necrosis factor (TNF-α) and brain-derived neurotrophic factor (BDNF) were examined by immunohistochemistry. Noradrenaline (NE) expression in plasma was evaluated by ELISA. The respiratory control ratio (RCR) of brain mitochondria was detected using a Clark oxygen electrode. Results: TCST effectively improved the cognitive function of TBI rats. TCST significantly inhibited sympathetic activity in the rats and effectively inhibited inflammatory responses. The expression of BDNF at T 1 -T 6 in TBI+TCST group was higher than that in TBI group ( P <0.05). Furthermore, P38 expression was inhibited more effectively in TBI+TCST group ( P <0.05), than in TBI group ( P <0.05), and the RCR of the brain was significantly higher in TBI+TCST group than in TBI group ( P <0.05). Conclusions: TCST can enhance cognitive function in TBI rats by inhibiting sympathetic activity, reducing inflammatory responses and brain edema, upregulating BDNF and improving brain mitochondrial function.

Effects of Massage on Neuro-Vascular Regulation and Apoptosis in Rabbits with Cervical Spondylosis of the Vertebral Artery Type

“…It has been found [27,28] that by inhibiting sympathetic excitability, serum NE levels can be reduced and the p38MAPK signaling pathway can be inhibited, causing intracellular reactive oxygen species (ROS) levels are reduced, thereby reducing the degree of endoplasmic reticulum stress (ERS) in the cell. Stellate ganglion blockade could also reduce ERS overactivation in arterial tissue by inhibiting sympathetic excitability, thereby improving vascular calci cation [29].The most important protective pathway of ERS is the unfolded protein response (UPR) [30], however, excessive ERS can lead to an imbalance in the regulatory capacity of the UPR and promote CHOP protein activity, which in turn induces apoptosis [31].…”

Imaging increased metabolism in the spinal cord in mice after middle cerebral artery occlusion

“…Cervical sympathetic trunk ischemia induced by bilateral common carotid artery ligation has been shown to lead to degeneration of the cervical sympathetic trunk, which inhibits sympathetic activity [98] . Cervical sympathetic trunk transection has been shown to lead to a decreased inflammatory response [99] . This would argue that cervical sympathetic trunk ischemia due to the tMCAO procedure should lead to a decrease in sympathetic activity and reduced hematopoietic bone marrow stem cell activity.…”