HYPERGLYCEMIA INDUCES INFLAMMATORY RESPONSE AND AGGRAVATES THE DEGREE OF ISCHEMIC BRAIN INJURY IN THE BODY THROUGH THE PPARΓ/NF-ΚB P65 SIGNALING PATHWAY

Pingli Wang^*, Yongsheng Wang 

Department of Neurology, Wenzhou City Hospital of Integrated Traditional Chinese and Western Medicine, Wenzhou 325000, PR China

Objective: To study the effect and mechanism of hyperglycemia on the degree of ischemic brain injury. 

Methods: 51 clean SD rats were randomly divided into a normal control group (17 cases), a non-diabetic group (17 cases), and a diabetic group (17 cases). Rats in the normal control group were fed a normal diet for 8 weeks, and chloral hydrate was injected into the abdominal cavity to separate the total neck, the internal neck, and the external neck A after complete anaesthetization. The rats in the non-diabetic group were fed normal feed for 8 weeks. After being fully anesthetized by chloral hydrate injection, the model of cerebral infarction was established by the Longa method. The rats were sacrificed after 24 hours of ischemia, and the serum and brain tissue were taken for testing. Rats in the diabetic group were intraperitoneally injected with 30mg·kg-1 of streptozotocin to establish type 2 diabetes after being fed a high-sugar and high-fat diet for 8 weeks. A blood glucose level of >16.7mmol/L was considered a success in the model. On this basis, the rat model of cerebral infarction was established by the Longa method. The rats were sacrificed after 24 hours of ischemia, and the serum and brain tissues were taken for testing. The levels of blood glucose and glycated hemoglobin (HbA1c) of rats in each group were observed and analyzed. The cerebral infarction area index, serum inflammatory-related factor levels [interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and C-reactive protein (CRP)], and NF-ΚB, PPARγ protein expression levels were compared.

Results: The blood glucose and HbA1c levels in the diabetic group were significantly higher than those in the normal control group (P<0.05) and were significantly higher than those in the non-diabetic group. The blood glucose and HbA1c levels in the non-diabetic group were not significantly different from those in the diabetic group (P>0.05). The cerebral infarction area indexes of the diabetic and non-diabetic groups were significantly higher than that of the normal control group, and that of the diabetic group was significantly higher than that of the non-diabetic group (P<0.05). The levels of TNF-α, IL-6 and CRP in the diabetic and non-diabetic groups were significantly higher than those in the normal control group (P<0.05), and those of the diabetic group were significantly higher than those of the non-diabetic group (P<0.05). The expression levels of NF-κB protein in the diabetic and non-diabetic groups were significantly higher than that in normal control group, and the levels of PPARγ protein expression were significantly lower than that in normal control group (P<0.05). The level of NF-κB protein expression in the diabetic group was significantly higher than that in the normal control group, and the level of PPARγ protein expression was significantly lower than that in the normal control group (P<0.05).

Conclusion: High blood sugar and high HbA1c can hinder the expression of PPARγ and promote the expression of NF-κB p65, leading to the massive release of inflammatory factors in the body; this ultimately leads to a further increase in the degree of ischemic brain damage.