Hyaluronic acid inhibits the glial scar formation after brain damage with tissue loss in rats.
BACKGROUND
Brain tissue scarring (gliosis) was believed to be the major cause of epileptic focus after brain injury, and prevention of scarring could reduce the incidence of seizure. We tried the HA coating onto the cortical brain defect of Spraque-Dawley rats to reduce the marginal glial scarring.


METHODS
A 4 x 2 x 2 mm(3) cortical defect was created in the brain of Spraque-Dawley rats. Three percent HA gel was coated onto the lesion for the experimental groups and normal saline solutions for the control groups. The brain was retrieved 4, 8, and 12 weeks after treatment. The brains were then sectioned and processed for H&E and GFAP staining, and the thickness of the scarring and the number of GFAP+ cells were analyzed.


RESULTS
The thickness of cutting marginal gliosis was significantly decreased in the HA groups. The 12-week HA group showed the smallest thickness of gliosis, whereas the 12-week control group exhibited the largest thickness of gliosis. The significant difference in the thickness of gliosis was also noted between the HA and the control groups 8 weeks after treatment. The number of GFAP+ cells was also significantly decreased in the HA groups when compared to the respective control group 4, 8, and 12 weeks after the surgery.


CONCLUSIONS
The results support the hypothesis that HA inhibits glial scarring not only by decreasing the thickness of gliosis but also by reducing the number of the glial cells. Furthermore, our results suggest that HA might be used to reduce glial scar formation in central nervous system surgery, which subsequently prevents the post-operation or posttraumatic seizure incidence.
Lin
Chien-Min
CM
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Lin
Jia-Wei
JW
Chen
Yen-Chou
YC
Shen
Hsin-Hsin
HH
Wei
Li
L
Yeh
Yi-Shian
YS
Chiang
Yung-Hsiao
YH
Shih
Raymond
R
Chiu
Pei-Ling
PL
Hung
Kuo-Sheng
KS
Yang
Liang-Yo
LY
Chiu
Wen-Ta
WT
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications* / Q000503:physiopathology; D002921:Cicatrix / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D004195:Disease Models, Animal; D004827:Epilepsy / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D005109:Extracellular Matrix / Q000187:drug effects / Q000378:metabolism; D005911:Gliosis / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D006820:Hyaluronic Acid / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016896:Treatment Outcome
D006820:Hyaluronic Acid