| ObjectiveIntracranial aneurysm(IA)which is a pathological abnormal bulging of the intracranial blood vessel wall,which usually occurs in the Willis artery or arterial bifurcation.The incidence rate is 3% in the human population.It is often occult disease in the cerebral blood vessels,but the tumor is dynamic.Changes,its initial symptoms are often catastrophic,so its exact incidence is not yet clear.Studies by scholars at home and abroad believe that intracranial aneurysms are the result of interactions of various factors,including hemodynamic factors,genetic factors,and inflammatory factors,among which hemodynamic factors play a role in the formation of aneurysms.Start with action..JNK can not only regulate the expression of Bax apoptotic protein in the process of intracranial aneurysm,but also regulate the growth of smooth muscle cells,the synthesis of extracellular matrix and the secretion of matrix metalloproteinases.In this study,the basal artery aneurysms of rabbits were induced by ligating bilateral common carotid arteries.The molecular mechanism of aneurysm onset was also investigated.Diamonium glycyrrhizinate was used to interfere with the expression of JNK and the phenotypic transition and apoptosis of smooth muscle cells were observed.The degradation of extracellular matrix provides scientific evidence and theoretical basis for the prevention of intracranial aneurysm formation.Methods40 experiment New Zealand white rabbits of clean grade weighing 2.5-3.8 kg were divided into 4 groups by random number table method.They were divided into normal control group(A group)10,surgical group(B group)10,surgery + saline There were 10 rats in the group(C)and 10 mice in the surgery + diammonium glycyrrhizinate group(D).Each group was divided into 4 subgroups(4w,8w,16 w,24w)according to the observation time points.The normal group was not treated.B,C,D groups were used to make rabbit apical aneurysm models by bilateral common carotid artery plus method.The non-intervention group received normal postoperative feeding and the diammonium glycyrrhizinate intervention group received 20 mg of diammonium glycyrrhizinate every 7 days after the model was established.The normal saline control group received only the same dose of normal saline every day.The intracranial vascular Doppler TCD and nuclear magnetic resonance angiography(MRA)were performed on each group of animal models at the time of grouping after surgery.The blood flow velocity and vascular diameter of the basilar arteries in each group were compared,and computer fluids were performed.The mechanical analysis(CFD)observed the variation of wall shear stress(WSS)in each group.Animal models were sacrificed by overdose of anesthesia.Basilar artery specimens were removed.Hemanyl-eosin(HE)staining was used to observe the morphology of the basilar arteries in each group.Masson staining was used to observe the change of the elastic layer in the basilar artery.Each group was observed by EVG staining.Basal artery wall elastic layer changes.The expression of JNK and Bax in each group was detected by immunohistochemistry.ResultsThe wall shear stress(wss)of the basilar artery was measured by computerhydrodynamics method.The wall shear stress of the basilar artery increased significantly after modeling compared with that before modeling(P<0.05).The wall shear stress of the normal control group(21.07±3.84);wall shear stress(52.27±4.92)at 2 weeks postoperatively;wall shear stress of(34.08±3.64)at 4 weeks postoperatively;group wall shear stress of group 8 weeks postoperatively(29.94)±1.87);The wall shear stress was(23.92±4.33)at 16 weeks postoperatively.Statistical analysis showed that there was no significant difference between the normal group and the 16-week group(P>0.05).There was a statistical difference between the normal group and the 2-week group(P<0.05).The normal group and the postoperative 4 weeks There was a statistically significant difference between the groups,and the difference between the normal group and the 8-week group was statistically significant(P<0.05).Histopathological staining after modeling showed destructive pathological remodeling of the basilar artery,including rupture of the internal elastic layer,thinning of the arterial media,and pathological outward swelling of the vessel.EVG staining showed that the elastic membrane in the normal control group was intact without any obvious damage.The average length of elastic membrane in group B was(171.15±26.87)μm.The C group was(173.99±31.12)μm,and the D group was(97.42±15.81)μm.The difference between group B and group D was statistically significant(P<0.05).The difference between group C and group D was statistically significant(P<0.05).As shown by Masson staining,the media layer became thin and partially stained with visible swelling of the vascular wall(Figure 5).In group A,no obvious thinning was observed.In the model group,there was a thinning of the layers in the arterial media.The average thinning length in group B was(148.08±19.17)μm,which was(143.00±19.37)μm in group C and(89.38±15.29)μm in group D.The degree of thinning was significantly reduced in group D compared with group B.Statistical significance(P<0.05).There was significant difference between D group and C group(P<0.05).Immunohistochemistry results of JNK group: A group:(17.70±3.59);B group(31.40±3.41);Group C(32.20±4.31);Group D:(23.60±4.06).The difference between group A and group B was statistically significant(P<0.05).There was a significant difference between group A and group D(P<0.05).There was no significant difference between group B and group C(P>0.05).There was a difference between group C and group D.Significant difference(P<0.05),B group and D group were significantly different(P <0.05).The immunohistochemical results of Bax in group A were(18.10±3.57);B(31.30±3.40);C:(32.70±3.57);D:(21.40±2.67).In statistical analysis,group A and group B had a statistical difference between(P<0.05).There was no significant difference between group B and group C(P>0.05).group C and group D had a statistical difference between P<0.05).There was a significant difference between group B and group D(P<0.05).Conclusions1.By ligating bilateral common carotid arteries in New Zealand white rabbits,a model of arterial cusp artery aneurysm in the basilar arteries can be made easily and easily,which can simulate the process of intracranial aneurysm formation caused by hemodynamic changes.After ligation of the intracranial aneurysm model,the vascular remodeling of the basilar arterial apex,rupture of the elastic membrane within the artery,thinning of the medial layer,and bulging outward of the vessel wall were changed.2.After modeling,the expression of JNK and Bax protein in the apical part of rabbit basilar artery was significantly increased,which promoted the phenotypic transition of vascular smooth muscle cells,apoptosis of smooth muscle cells and degradation of extracellular matrix.3.Diammonium glycyrrhizinate can play an important role in inhibiting the formation of intracranial aneurysms by inhibiting the expression of JNK,down-regulating the expression of Bax protein in the arterial media,inhibiting the degradation of extracellular matrix and pathological reconstruction of vascular wall. |
