History and Mechanism for Treatment of Intracerebral Hemorrhage with Scalp Acupuncture

Table 4

Possible mechanisms for treatment of acute ICH with scalp acupuncture.

Possible targets	Possible mechanisms
Influence on hematoma, brain edema and, blood brain barrier	Improve the absorption rate of hematoma, reduce brain edema, diminish cerebral vessel permeability, and promote reparation for BBB damage.
Influence on the products released from haematoma	Inhibit the expression of MMP-9, AQP-4, and PAR-1.
Influence on the immune and inflammatory reaction	Inhibit the expression of IL-1β, decrease serum IL-6 level, inhibit TNF-α expression, and promote HSP70 expression. Increase CD3 and CD4/CD8 level, while decreasing CD8 level.
Influence on focal perihemorrhagic hypoperfusion and hemorheology	improve energy metabolism, upregulate the activity of hondriosome (Succinate dehydrogenase and Na^+-K^+-ATPase), reduce the accumulation of lactate acid, delay Glut-1 expression, lower plasma ET level and NSE level, and heighten CGRP level.
Influence on neuroelectrophysiology	Relieve the inhibitive generalization of the whole brain neuron function, have bidirectional and beneficial regulation effect on electric activity of pain-reaction neurons, and recover abnormal SEPs.
Others	Promote the NCF gene expression, promote the expression of endogenous GDNF, lower the level of serum S-100B, and promote the level of IGF-1.

BBB, blood-brain barrier. MMP-9, matrix metallopeptidase-9. AQP-4, aquaporin-4. PAR-1, protease-activated receptor-1. IL, interleukin. TNF-α, tumour necrosis factor α. HSP70, heat shock protein 70. Glut-1, glucose transporter-1. ET, endothelin. NSE, neuron specific enolase. CGRP, calcitonin gene-related peptide. SEPs, somatosensory-evoked potentials. NCF, nerve growth factor. GDNF, glial cell line-derived neurotrophic factor. IGF-1, insulin-like growth factor 1.