Expermental Study Of Treatment On Diabetic Cerebral Infarction With Yi-Xao-Fu-Tan Decoction

Objective： Study the pathology mechanism and treatment method of cerebralinfarction with diabetic,we put forward the main pathology mechanism "qi deficiency andblood stasis,stasis heat reducing toxicant,toxicant damaging brain collaterals". So thetreatment methods of clearing away heat and toxic materials and supplementing qi andactivating blood circulation maybe a valid therapy,and Yi-Xiao-Fu-tan decoction(YXFTT)maybe valid treatment drug. We investigated the changes and the molecular mechanisms ofcerebral vascular damage and tested the therapeutic effects of YXFTT in diabetic rats afterstroke.Methods: Male Sprague-Dawley rats were fed with high fat and high sugar diet for4weeks,then injected intraperitoneally with low dose of streptozotocin (STZ)(30mg/kg)serves as an alternative animal model for type2diabetes,the diabetes rats (blood glucose≥16.7mmol/L)then underwent permanent middle cerebral artery occlusiont.we treated thestroke rats in diabetic with YXFTT for a week, at the same time,we set sham group,MCAOwithout diabetic group,diabete group with sham operation group to control. Neurologicfunction,cerebral infarct volume, brain water content,myeloperoxidase (MPO) activity andhippocampal CA1neurons injury were measured24h after MCAO. Expression ofTLR4,and the downstream effector molecules tumor necrosis factor-alpha (TNF-α) andinterleukin-1beta (IL-1β) were determined by western blot.Results: The stroke rats with diabetes showed significantly higher mortality, biggerinfarcts, increased cerebral edema, worsened neurological status compared to rats withoutdiabtes. The diabetes rats also showed significantly higher post-ischemic inflammatorymarkers MPO activity, exacerbated proinflammatory gene expression compared to rats without diabetes. In addition, the post-ischemic neuroprotective YXFTT reduced cerebralinfarct area and infarct volume. YXFTT reduced the expression of TLR4and TNF-α andIL-1β. Our results suggest that YXFTT inhibits the TLR4signaling pathway in cerebralischemia with diabetes, which may be a mechanism underlying the YXFTT’sneuroprotection.Conclusions: With high fat and high sugar diet combined with small dose injection ofSTZ,then underwent permanent middle cerebral artery occlusion can be successfullyestablished based on diabetic cerebral infarction model, YXFTT in experiments withdiabetic cerebral infarction can reduce nerve damage, reduce the expression of TLR4signaling pathway, play a protective role.