Bloodletting Puncture at Hand Twelve Jing-Well Points Relieves Brain Edema after Severe Traumatic Brain Injury in Rats via Inhibiting MAPK Signaling Pathway.
10.1007/s11655-021-3326-5
- Author:
Bao-Hu LIU
1
;
Dan ZHOU
1
;
Yi GUO
1
;
Sai ZHANG
2
;
Yong-Ming GUO
1
;
Tong-Tong GUO
3
;
Xu-Yi CHEN
2
;
Yi-Nan GONG
1
;
Hui-Ling TANG
1
;
Zhi-Fang XU
4
Author Information
1. Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China.
2. Tianjin Key Laboratory of Neurotrauma Repair, Institution of Brain Trauma and Neurology Disease of People's Armed Police Force, Neurosurgery & Neurology Hospital, Affiliated Hospital of Logistics University of People's Armed Police Force, Tianjin, 300162, China.
3. College of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China.
4. Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China. xuzhifangmsn@hotmail.com.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
blood brain barrier;
bloodletting puncture at hand twelve Jing-well points;
cerebral edema;
mitogen-activated protein kinase pathway;
traumatic brain injury
- From:
Chinese journal of integrative medicine
2021;27(4):291-299
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate whether blood-brain barrier (BBB) served a key role in the edema-relief effect of bloodletting puncture at hand twelve Jing-well points (HTWP) in traumatic brain injury (TBI) and the potential molecular signaling pathways.
METHODS:Adult male Sprague-Dawley rats were assigned to the sham-operated (sham), TBI, and bloodletting puncture (bloodletting) groups (n=24 per group) using a randomized number table. The TBI model rats were induced by cortical contusion and then bloodletting puncture were performed at HTWP twice a day for 2 days. The neurological function and cerebral edema were evaluated by modified neurological severity score (mNSS), cerebral water content, magnetic resonance imaging and hematoxylin and eosin staining. Cerebral blood flow was measured by laser speckles. The protein levels of aquaporin 4 (AQP4), matrix metalloproteinases 9 (MMP9) and mitogen-activated protein kinase pathway (MAPK) signaling were detected by immunofluorescence staining and Western blot.
RESULTS:Compared with TBI group, bloodletting puncture improved neurological function at 24 and 48 h, alleviated cerebral edema at 48 h, and reduced the permeability of BBB induced by TBI (all P<0.05). The AQP4 and MMP9 which would disrupt the integrity of BBB were downregulated by bloodletting puncture (P<0.05 or P<0.01). In addition, the extracellular signal-regulated kinase (ERK) and p38 signaling pathways were inhibited by bloodletting puncture (P<0.05).
CONCLUSIONS:Bloodletting puncture at HTWP might play a significant role in protecting BBB through regulating the expressions of MMP9 and AQP4 as well as corresponding regulatory upstream ERK and p38 signaling pathways. Therefore, bloodletting puncture at HTWP may be a promising therapeutic strategy for TBI-induced cerebral edema.
