Effects Of Total Glycosides Of Cistanche On O Xidative Stress Injury And Apoptosis in Rats With Cerebral Ischemia - Reperfusion Ⅱ

2 results

2． 1 Comparison of neurological deficit scores 

Compared with the Sham group, rats in the Mod⁃el group had more severe neurological deficit symptoms and increased neurological deficit scores (P ＜0. 05); compared with the Model group, the rats in the GCs group had higher The neurological deficit score decreased (P <0. 05), see Figure 1.

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2． 2 TTC staining results of brain tissue

There were no obvious infarction lesions in the brain tissue of the rats in the Sham group. In comparison, the percentage of cerebral infarction area in the rats in the Model group was larger (P < 0.01); the percentage of cerebral infarction area in the rats in the GCs treatment group was lower than that in the Model group. (P <0. 05), see Figure 2.

2． 3 Comparison of oxidative stress indicators

Compared with the Sham group, the MDA content in the serum of rats in the Model group increased, and the activities of the antioxidant factor SOD and GSH-Px decreased (P < 0.05); while the rats in the GCs group compared with the M group Rats in the odel group, The MDA content decreased, and the activities of SOD and GSH-Px increased (P < 0. 05), see Table 1.

3 Discussion

It is known that multiple factors and multiple links are involved in the subsequent nerve cell necrosis caused by CIRI. Inhibiting the occurrence and development of the pathological process within an effective period of time is extremely critical for the prognosis of the disease. Wang et al. [4] published Figure 3. Comparison of Bax, Bcl-2, Caspase-3, HO-1, and Nrf2 protein expression in the brain tissue of rats in each group. Note: Compared with the sham operation group, ∗ Ｐ＜0. 0５,∗∗Ｐ＜0． 01; compared with the model group, #P < 0. 0５,##P＜0. 01 The improvement of neurological deficit and cerebral infarction area of CIRI rats after GCs treatment has confirmed its effect on brain tissue damage and post-morbidity movement.

The positive effect of recovery of motor function; the results of this experiment also proved that the neurological deficit score of rats after CIRI treatment with GCs was reduced, and the percentage of brain tissue infarction area was reduced, suggesting that GCs has a protective effect on brain damage after CIRI.

As an important regulatory factor involved in redox reactions in cells, Nrf 2 plays an important role in the occurrence of many diseases, such as neurodegenerative diseases, tumors, aging, etc. 9].

  It exerts its antioxidant effect by combining with anti-oxidant response elements (ARE) to promote downstream SOD, Expression of CAT and GSH-Px [10]. HO-1 serves as a regulatory protein of the Nrf 2/ARE pathway, and its activation can initiate anti-oxidative stress, anti-inflammatory, and

Protective mechanism against cell damage[11]. HO-1 can promote the oxidative degradation of heme and neutralize excess reactive oxygen species. Its upregulation is an important mechanism for cells to adapt to oxidative stress. HO-1 can resist the damage caused by oxidative stress to the body, thereby reducing cell apoptosis [12].

After CIRI occurs, the excessive production of oxygen free radicals will lead to an imbalance in their production and degradation, and the accumulation of reactive oxygen species will cause cells to be attacked by excessive reactive oxygen species. SOD and GSH-Px are important antioxidant factors, and their absence can promote lipid peroxidation, and the production of the cytotoxic substance MDA will further increase, resulting in a series of cell dysfunctions and aggravating brain damage [13].

Wang et al. [14] found that by increasing the activities of SOD, CAT and GSH-Px and reducing the content of MDA and protein hydroxyl groups, the antioxidant capacity of serum, liver and brain can be improved. Ye Hongxia et al. [15] found in a study on the nootropic effect of GCs on mice that it reduced the damage to brain tissue structure and function by increasing antioxidant enzyme activity and reducing oxidative stress levels. Previous studies by Wang et al. [4] confirmed that GCs treatment promotes neuronal remodeling and angiogenesis. The mechanism may be related to activating the Nrf 2 pathway and reducing the oxidative stress level of brain tissue. The results of this experiment showed that GCs up-regulated the expression of Nrf 2 and its downstream target protein HO-1, increased the activity of antioxidant enzymes SOD and GSH-Px in brain tissue, accelerated the scavenging of oxygen free radicals, and also reduced cytotoxicity. The accumulation of the substance MDA, thereby reducing oxidative stress-induced brain damage.

Wu Jiangli et al. [16] have shown that Nrf 2 can also directly regulate the mitochondria-mediated endogenous apoptosis pathway, regulate the expression of proteins Bax and Bcl-2 and inhibit apoptosis. Studies have found that GCs can significantly up-regulate the expression of Bcl-2 in myocardial tissue, down-regulate the expression of Bax and Caspase-3, reduce apoptosis caused by ischemia-reperfusion, and thereby reduce myocardial damage [17].

In studies on the effects of GCs on tumor growth and metastasis, it was found that they exert a pro-apoptotic effect by regulating the expression of Bax and Bcl-2 proteins. After the proliferation of endothelial cells is inhibited, the formation of blood vessels is also reduced [18] . The results of this experimental study showed that GCs intervention increased the expression of the anti-apoptotic protein Bcl-2 and reduced the expression of the pro-apoptotic proteins Bax and Caspase-3 in brain tissue, fully proving that it positively promotes the survival of nerve cells. effect.

In summary, GCs may improve the ability of nerve cells in the ischemic penumbra area to resist oxidative stress damage and reduce nerve cell apoptosis caused by CIRI by activating the Nrf 2/HO-1 pathway, suggesting that GCs may be a kind of Potential drugs for the treatment of cascade brain injury after cerebral ischemia-reperfusion.

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