Original Article
Wogonin improves functional neuroprotection for acute cerebral ischemia in rats by promoting angiogenesis via TGF-β1
Abstract
Background: Previous studies showed that wogonin is a potential candidate for more effective treatment of neuronal and inflammatory disease and could offer neuroprotective activity in various models, but all these studies were in vitro. Our research aimed to investigate the neuroprotective effect of wogonin on focal cerebral ischemia in rats and uncover its potential mechanism.
Methods: A total of 80 male SD rats were randomly divided into a sham operation group (Sham group, 20 rats), a normal saline group (NS group, 20 rats), and a wogonin intervention group (W2W group, 20 rats), while the remaining 20 rats were kept as a substitute. The model of focal cerebral ischemia (MCAO) was established by thread embolization. The neurological deficits were evaluated by the modified neurological deficit scale (mNSS). The laser confocal technique was used to observe the diameter, density, and total area of microvessel. Lastly, the expression of transforming growth factor-β1 (TGF-β1) was detected by Western blot.
Results: The mNSS scores of the NS group and Wn2W group were 6.57±1.13 and 4.39±0.92 respectively, and the difference between NS group and Wn2W group was statistically significant (P<0.05); the vascular diameter of the Wn2W group, Sham group, and NS group were 2.93±0.19, 4.24±0.16, and 3.56±0.22 µm respectively, and the differences among these groups were statistically significant (F=102.142, P<0.01). Furthermore, the differences in the vascular density (F=290.49, P<0.01) and total microvessel area (F=163.08, P<0.01) among these groups were also statistically significant. The expression of TGF-β1 in ischemic brain tissue of the Sham group, NS group, and Wn2W group were 0.46±0.14, 0.62±0.18, and 0.94±0.21 respectively, and the differences among these groups were statistically significant (F=102.142, P<0.01).
Conclusions: Wogonin can markedly reduce nerve injury and improve nerve function in rats with cerebral ischemia, which may be related to the TGF-β1 pathway.
Methods: A total of 80 male SD rats were randomly divided into a sham operation group (Sham group, 20 rats), a normal saline group (NS group, 20 rats), and a wogonin intervention group (W2W group, 20 rats), while the remaining 20 rats were kept as a substitute. The model of focal cerebral ischemia (MCAO) was established by thread embolization. The neurological deficits were evaluated by the modified neurological deficit scale (mNSS). The laser confocal technique was used to observe the diameter, density, and total area of microvessel. Lastly, the expression of transforming growth factor-β1 (TGF-β1) was detected by Western blot.
Results: The mNSS scores of the NS group and Wn2W group were 6.57±1.13 and 4.39±0.92 respectively, and the difference between NS group and Wn2W group was statistically significant (P<0.05); the vascular diameter of the Wn2W group, Sham group, and NS group were 2.93±0.19, 4.24±0.16, and 3.56±0.22 µm respectively, and the differences among these groups were statistically significant (F=102.142, P<0.01). Furthermore, the differences in the vascular density (F=290.49, P<0.01) and total microvessel area (F=163.08, P<0.01) among these groups were also statistically significant. The expression of TGF-β1 in ischemic brain tissue of the Sham group, NS group, and Wn2W group were 0.46±0.14, 0.62±0.18, and 0.94±0.21 respectively, and the differences among these groups were statistically significant (F=102.142, P<0.01).
Conclusions: Wogonin can markedly reduce nerve injury and improve nerve function in rats with cerebral ischemia, which may be related to the TGF-β1 pathway.
