Guillain-Barre syndrome after myocardial infarction: a case report and literature review.

BACKGROUND: Guillain-Barre syndrome after myocardial infarction occurs infrequently, and its occurrence following percutaneous coronary intervention is extremely rare. Due to the high mortality rate of myocardial infarction and the disability of Guillain-Barre syndrome, early identification of Guillain-Barre syndrome after myocardial infarction and early intervention can decrease the mortality rate, lead to early recovery, and provide a better outcome. CASE PRESENTATION: Herein, we reported a rare case of Guillain-Barre syndrome after myocardial infarction treated with percutaneous coronary intervention. The patient was a 75-year-old woman from China who was admitted to hospital due to sudden loss of consciousness. Electrocardiography showed acute myocardial infarction in the right ventricle and inferior and posterior walls. The patient underwent emergency percutaneous intervention of the posterior collateral artery of the right coronary artery. Soon after, her condition worsened resulting in limb weakness and numbness. Unfortunately, she continued to develop respiratory failure, and treated with intravenous immunoglobulin and ventilator-assisted breathing. A physical examination showed hypotonia of all four limbs, complete quadriplegia, bulbar palsy, dysarthria, and tendon areflexia. Serum immunoglobulin (Ig) G anti-ganglioside antibody analysis was positive with anti-GT1a antibodies (+ +), anti-GM1 antibodies ( +), anti-GM2 antibodies ( +), and anti-GM4 antibodies ( +), and he was diagnosed with Guillain-Barre syndrome after myocardial infarction. She was discharged due to poor response to treatment. The patient died two days after being discharged. CONCLUSIONS: Myocardial infarction and/or percutaneous coronary intervention may activate immune-mediated response and cause severe complications. Clinician should be alert to Guillain-Barre syndrome after myocardial infarction and/or percutaneous coronary intervention.

A case report of autoimmune GFAP astrocytopathy presenting with abnormal heart rate variability and blood pressure variability.

BACKGROUND: Autonomic dysfunctions including bladder dysfunction, gastrointestinal dysfunction and orthostasis are common symptoms of autoimmune glial fibrillary acidic protein astrocytopathy (A-GFAP-A); however, cardiac autonomic dysfunction and abnormal circadian rhythm of blood pressure, which can lead to poor prognosis and even sudden cardiac death, has never been reported in A-GFAP-A patient. CASE PRESENTATION: A 68-year-old male Chinese patient presented to our hospital with headache, fever, progressive disturbance of consciousness, dysuria, and limb weakness. Abnormal heart rate variability and non-dipper circadian rhythm of blood pressure gradually developed during hospitalization, which is rare in A-GFAP-A. He had positive GFAP IgG in cerebrospinal fluid (CSF). Enhanced brian MRI showed uneven enhancement and T2 hyperintense lesions of medulla oblongata; Cervical spine MRI showed T2 hyperintense lesions in medulla oblongata and upper margin of the T2 vertebral body. A contrast-enhanced thoracic spine MRI showed uneven enhancement and T2 hyperintense lesions of T1 to T6 vertebral segments. After treatment with intravenous immunoglobulin and corticosteroids, the patient's symptoms, including autonomic dysfunction, alleviated dramatically. Finally, his heart rate variability and blood pressure variability became normal. CONCLUSIONS: Our case broadens the spectrum of expected symptoms in A-GFAP- A syndromes as it presented with heart rate variability and blood pressure variability.

Tanshinone IIA increases levels of NeuN, protein disulfide isomerase, and Na+/K+-ATPase and decreases evidence of microglial activation after cerebral ischemic injury.

This study was designed to clarify the neuroprotective effects of tanshinone IIA (TSA) following cerebral ischemic insult. Adult Sprague-Dawley rats were operated upon to achieve a middle cerebral artery occlusion to cause transient focal cerebral ischemia, which were then randomly divided into the sham-operated control group and cerebral ischemia/reperfusion (I/R) groups receiving a 2 h occlusion. The treatment groups received daily intraperitoneal injections of high or low doses of TSA, for 7 or 15 days. NeuN immunostaining revealed neuronal loss following I/R, which was partially prevented with subsequent TSA dosing. Protein disulfide isomerase and adenosine triphosphatase (Na(+)/K(+)-ATPase) levels were all depressed by means of I/R. TSA treatment markedly reversed the depression of all indices examined. The intensity of microglial activation, as evidenced with CD11b staining, was increased by means of cerebral artery occlusion, but this was partially reversed with subsequent TSA treatment. TSA may affect neuroprotection by way of minimizing deficits in energy metabolism and reduction of the extent of cell death within affected regions.

Upregulation effects of Tanshinone IIA on the expressions of NeuN, Nissl body, and IκB and downregulation effects on the expressions of GFAP and NF-κB in the brain tissues of rat models of Alzheimer's disease.

This study aimed to observe the effects of Tanshinone IIA(Tan IIA) treatment on the expression levels of brain tissue NeuN, Nissl body, IκB, GFAP and NF-κB in Alzheimer's disease (AD) rats to explore the possible anti-inflammatory and neuroprotective mechanisms of Tan IIA. Thirty healthy male Sprague-Dawley rats were randomized into three groups: Sham group, AD+vehicle control group, and AD+Tan IIA group. The models of AD were established by injecting Aß1-42 into the hippocampus of rats. Tagged position and the expression levels of Aß1-42 were observed by immunohistochemistry staining to prove the success of the model of AD. Brain tissues of all groups were collected after Tan IIA treatment and paraffin sections were prepared to assess pathological changes and expression levels of GFAP, IκB and NF-κB by both immunohistochemistry and western blotting. After Aß1-42 injection, the expression levels of GFAP and NF-κB were significantly stronger in the AD+vehicle control group than those in the AD+Tan IIA group and the sham group (P<0.05), the IκB expression level and the number of neurons and Nissl bodies of AD+vehicle control group was reduced compared with the sham or the AD+Tan IIA group (P<0.05). In conclusion, Aß induces a cerebral tissue inflammation reaction. Tan IIA treatment can suppress the proliferation of astrocytes in an AD model, lower the level of NF-κB, and increase the level of NeuN, Nissl body, IκB, thus exerting anti-inflammatory and neuroprotective effects.

Protective effect of Tanshinone IIA against infarct size and increased HMGB1, NFκB, GFAP and apoptosis consequent to transient middle cerebral artery occlusion.

Acute inflammation plays an important role in brain damage following cerebral ischemia and reperfusion (I/R) injury. The present study employed a rat model of middle cerebral artery occlusion to explore the neuroprotective effects of tanshinone IIA (TSN), which is widely used in China for treating cerebrovascular and cardiovascular diseases. Rats were divided into a sham-operated group and I/R transiently occluded then reperfused groups. Some of the I/R animals were treated daily for 7 or 15 days with two different doses of TSN. After 15 days, triphenyl tetrazolium chloride staining revealed less unstained area indicating fewer lesions in the TSN-treated I/R group relative to the untreated corresponding I/R group. TSN treatment dramatically reduced infarct sizes and reduced content of high mobility group box 1 protein following I/R. Nuclear translocation of NFκB was also attenuated in I/R animals subsequently receiving TSN. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining revealed more apoptosis in the I/R model group and this was reduced in the I/R animals treated with TSN for 15 days. Thus, TSN mitigates the severity of damage effected by I/R.

[Nuclear factor κB and IKB expression and calcium deposition of atherosclerotic plaques in apolipoprotein E and low density lipoprotein receptor knockout mice].

OBJECTIVE: To observe the histopathological features, nuclear factor-κB (NFκB) and IKB expressions as well as calcium deposition of atherosclerosis plaques (AS) in apolipoprotein E (ApoE) and low density lipoprotein receptor (LDLR) knockout mice (ApoE(-/-), LDLR(-/-)fed high-fat diet. METHODS: Eight C57BL/6J mice fed with normal diet were used as control, 32 ApoE(-/-) mice and LDLR(-/-) mice were divided into normal diet and high-fat diet groups (n = 8 each). After 4 months, aorta was collected for morphologic (HE, Oil Red O, Von Kossa) and immunohistochemistry (nuclear factor-κB, IKB, macrophage surface molecule-3, α-smooth action protein) analysis. RESULTS: Degree of AS in ApoE(-/-) and LDLR(-/-) mice fed with high-fat diet were significantly severer than those fed with normal diet and AS was more significant in ApoE(-/-) mice than in LDLR(-/-) mice. NFκB and IKB expressions in high-fat diet group were significantly higher than the normal diet group (P < 0.05). Double-labeling of NFκB revealed dominant expression in smooth muscle cells. Calcium deposition was significantly more in ApoE(-/-) mice fed with high-fat diet than mice fed with normal diet (P < 0.05) and was similar in LDLR(-/-) mice fed with high and normal diet (P > 0.05). CONCLUSION: High-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.

[Study on regulation of tanshinone II(A) on GFAP and ATPase and PDI of cerebral ischemia reperfusion injury in rats].

OBJECTIVE: To observe the neuroprotective effect of tanshinone II(A) (Tan II(A)) on the expression of brain tissue glial fibrillary acidic protein (GFAP) and adenosine triphosphatase (ATPase) and protein disulfide isomerase (PDI) of cerebral ischemia reperfusion (I/R) injury of different time in rats, and investigate the neuroprotective and its molecular mechanism of Tan II(A) on brain injury. METHODS: Sixty-four male Sprague-Dawley rats were randomly devided into eight groups (n = 8 per group): Group 1, sham-operated animals without I/R; Group 2, animals with I/R of 3 days; Group 3, animals with I/R of 7 days; Group 4, animals with I/R of 7 days and treatment with low doses of Tan II(A); Group 5, animals with IR of 7 days, treated with high doses of Tan II(A); Group 6, animals with I/R of 15 days; Group 7, animals with IR of 15 days and low doses of Tan II(A) treatment; Group 8, animals with I/R of 15 days, treated with high doses of Tan II(A). The model of focal middle cerebral artery occlusion (MCAO) was established by suture-occluded method. After Tan II(A) treatment, pathological changes of brain tissue in all groups were observed by hematoxylin-eosin staining (HE) and the expression levels of GFAP, ATP and PDI by immunohistochemistry staining. RESULTS: (1) The pathological changes of ischemic injury in low and high dose of Tan II(A) treatment groups were lighter than those in I/R groups, and so were in high dose of Tan II(A) treatment group than in low dose Tan II(A) treatment group. (2) Compared with sham-operated group, expression levels of GFAP in the three different I/R groups increased evidently, while the levels in high dose of Tan II(A) treatment groups were relatively low (P < 0.05). There was no statistically difference between high dose of Tan II(A) treatment group and low dose of Tan II(A) treatment group in either 7 or 15 days treatment groups (P > 0.05). (3) Compared with sham-operated group, expression levels of ATPase and PDI in the three different I/R groups all decreased clearly; Compared with I/R groups, expression levels of ATPase and PDI in Tan II(A) treatment groups increased in the ischemic territory obviously (P < 0.05). CONCLUSIONS: Tan II(A) may have a neuroprotective effect on ischemia-reperfusion injury by inhibiting the production of GFAP to reduce the excessive inflammatory response produced by glial cells in brain and up-regulating the activities of ATPase and PDI in neurons to improve the balance of energy metabolism and maintain the intracellular homeostasis.