Damage of hippocampal neurons in rats with chronic alcoholism

Chronic alcoholism can damage the cytoskeleton and aggravate neurological deficits. However, the effect of chronic alcoholism on hippocampal neurons remains unclear. In this study, a model of chronic alcoholism was established in rats that were fed with 6% alcohol for 42 days. Endogenous hydrogen sulfide content and cystathionine-beta-synthase activity in the hippocampus of rats with chronic alcoholism were significantly increased, while F-actin expression was decreased. Hippocampal neurons in rats with chronic alcoholism appeared to have a fuzzy nuclear mem- brane, mitochondrial edema, and ruptured mitochondrial crista. These findings suggest that chronic alcoholism can cause learning and memory decline in rats, which may be associated with the hydrogen sulfide/cystathionine-beta-synthase system, mitochondrial damage and reduced expression of F-actin.

Aminooxyacetic acid improves learning and memory in a rat model of chronic alcoholism

Chronic alcoholism seriously damages the central nervous system and leads to impaired learning and memory.Cell damage in chronic alcoholism is strongly associated with elevated levels of hydrogen sulfide（H2S） and calcium ion overload.Aminooxyacetic acid is a cystathionine-β-synthase activity inhibitor that can reduce H2S formation in the brain.This study sought to observe the effect of aminooxyacetic acid on learning and memory in a chronic alcoholism rat model.Rats were randomly divided into three groups.Rats in the control group were given pure water for 28 days.Rats in the model group were given 6% alcohol for 28 days to establish an alcoholism rat model.Rats in the aminooxyacetic acid remedy group were also given 6% alcohol for 28 days and were also intraperitoneally injected daily with aminooxyacetic acid（5 mg/kg） from day 15 to day 28.Learning and memory was tested using the Morris water maze test.The ultrastructure of mitochondria in the hippocampus was observed by electron microscopy.H2S levels in the hippocampus were measured indirectly by spectrophotometry,and ATPase activity was measured using a commercial kit.The expression of myelin basic protein was determined by immunohistochemistry and western blotting.Compared with the control group,latency and swimming distance were prolonged in the navigation test on days 2,3,and 4 in the model group.In the spatial probe test on day 5,the number of platform crosses was reduced in the model group.Cristae cracks,swelling or deformation of mitochondria appeared in the hippocampus,the hippocampal H2S level was increased,the mitochondrial ATPase activity was decreased,and the expression of myelin basic protein in the hippocampus was down-regulated in the model group compared with the control group.All the above indexes were ameliorated in the aminooxyacetic acid remedy group compared with the model group.These findings indicate that aminooxyacetic acid can improve learning and memory in a chronic alcoholism rat model,which may be associated with reduction of hippocampal H2S level and mitochondrial ATPase activity,and up-regulation of myelin basic protein levels in the hippocampus.

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

AIM: To study the possible association between chronic pancreatitis (CP) and liver cirrhosis (LC) of alcoholic etiology,after excluding any other causes.METHODS: One hundred and forty consecutive alcoholic patients were subdivided into three groups: CP (n = 53),LC (n = 57),and asymptomatic alcoholic (n = 30).Clinical,biochemical and morphological characteristics,Child-Pugh index,indocyanine green test,and fecal pancreatic elastase-1 test were assessed.RESULTS: In patients with cirrhosis,major clinical manifestations of CP such as pancreatic pain and steatorrhea,as well as imaging alterations of CP such as calcifications,duct dilation and pseudocysts were absent; insulin-dependent diabetes was present in 5.3% of cases,and elastase-1 test was altered in only 7%,and severely altered in none.In patients with CP,clinical characteristics of cirrhosis such as ascites,encephalopathy and gastrointestinal hemorrhage were present in one case,Child-Pugh grade > A in 5.7%,and altered indocyanine green test in 1.9% cases.In asymptomatic alcoholism,there was only a non-coincident alteration of elastase-1 test and indocyanine test in 14.8% and 10%,respectively,but other characteristics of cirrhosis or CP were absent.An inverse correlation (r = -0.746) between elastase-1 test and indocyanine test was found in alcoholic patients.CONCLUSION: There is a scarce coincidence in clinical and morphological alterations among patients with CP or LC of alcoholic etiology,but an inverse correlation between pancreatic and liver function tests.These findings support that these alcoholic diseases evolve in a different manner and have different etiopathogenesis.

Polyvinyl alcohol and gelatin sponge particle embolization of splenic artery pseudoaneurysm complicating chronic alcoholic pancreatitis

AIM:To assess the effectiveness of and complications associated with polyvinyl alcohol (PVA) and gelatin sponge particles embolization of splenic artery pseudoaneurysm complicating chronic alcoholic pancreatitis. METHODS: A 42-year-old man with splenic artery pseudoaneurysm formation secondary to chronic alcoholic pancreatitis was admitted. We used PVA and gelatin sponge particles embolization of splenic artery pseudoaneurysm by super-selective embolization techniques. RESULTS: The splenic artery pseudoaneurysm was successfully controlled with splenic embolization. The patient was discharged in 9 d with complete recovery. CONCLUSION: This case confirms that superselective transcatheter embolization by PVA and gelatin sponge particles may represent an effective treatment for pseudoaneurysm caused by chronic alcoholic pancreatitis in the absence of other therapeutic alternatives.

Alcohol,inflammation,and gut-liver-brain interactions in tissue damage and disease development

Chronic inflammation is often associated with alcoholrelated medical conditions. The key inducer of such inflammation, and also the best understood, is gut microflora-derived lipopolysaccharide (LPS). Alcohol can significantly increase the translocation of LPS from the gut. In healthy individuals, the adverse effects of LPS are kept in check by the actions and interactions of multiple organs. The liver plays a central role in detoxifying LPS and producing a balanced cytokine milieu. The central nervous system contributes to anti-inflammatory regulation through neuroimmunoendocrine actions. Chronic alcohol use impairs not only gut and liver functions, but also multi-organ interactions, leading to persistent systemic inflammation and ultimately, to organ damage. The study of these interactions may provide potential new targets for therapeutic intervention.