Liver Cell Necrosis Research Articles

Vitamin U alleviates AFB1-induced hepatotoxicity in pregnant and lactating mice by regulating the Nrf2/Hmox1 pathway

This study investigated the protective effect of Vitamin U on liver injury induced by aflatoxin B1 (AFB1) in maternal mice. 25 pregnant ICR mice were randomly divided into five groups: the AFB1 group (AF, 0.3 mg AFB1/kg b.w.), the Vitamin U group (U, 50 mg Vitamin U/kg b.w.), the AFB1 + Vitamin U group (AU, 50 mg Vitamin U /kg b.w. + 0.3 mg AFB1/kg b.w.), the control group (DMSO), and the MOCK group (distilled water). They were administered substances by gavage every day for 28 days. Results indicated that exposure to AFB1 increased the liver index and caused histological disruptions. Elevated serum levels of ALT and ALP were observed, along with a significant increase in liver MDA content and a decrease in GSH-Px and T-SOD levels. Moreover, the Keap1 and Hmox1 gene was downregulated with statistical significance, while the IL1β and TNFα gene were significantly upregulated. Vitamin U was demonstrated by the organized structure of liver cells in tissue slices, effectively reducing liver cell necrosis. This intervention was associated with a significant decrease in serum ALT and ALP activities, as well as a significant decrease in liver MDA content. Additionally, there were significant increases in liver T-SOD and GSH-Px levels, along with upregulation of mRNA and protein expression of Nfr2, Hmox1 and Keap1, and downregulation of mRNA expression of the IL1β gene. In summary, Vitamin U mitigated oxidative stress-induced liver injury by modulating the Nrf2/Hmox1 signaling pathway and inflammatory factors affected by AFB1.

Liver damage and lipid metabolic dysregulation in adult zebrafish (Danio rerio) induced by spirotetramat

Spirotetramat, an insecticide derived from cycloketone and extensively utilized in agricultural production, has been reported to be toxic to an array of aquatic organisms. Previous studies have indicated that spirotetramat can cause toxicity such as impaired ovarian development and apoptosis in zebrafish, but its toxicological effects on lipid metabolism and liver health in zebrafish remain unclear. In this study, we explored the effects of spirotetramat exposure on zebrafish (Danio rerio) by examining key markers of lipid metabolism, alterations in gene expression related to this process, and histological characteristics of the liver. Spirotetramat significantly reduced the condition factor, triglycerides and low-density lipoprotein cholesterol levels at 2 mg/L. The expression of genes related to fatty acid synthesis (acacb), β-oxidation (acox1, pparda) and pro-inflammatory cytokines (tnf-α, il-1β) was downregulated. However, the expression of genes related to lipid transport and uptake (cd36, ppara) and output (apob) was upregulated. The activity of alanine aminotransferase was significantly inhibited. Histopathology results showed that spirotetramat exposure led to liver cell vacuolation and necrosis. In addition, molecular docking results of spirotetramat and lipid transport related protein (ACC, ApoB) in both zebrafish and human showed the binding energy of human proteins is lower than that for zebrafish, and that the number of hydrogen bonds formed was higher. It is speculated that spirotetramat may also pose a significant potential hazard to humans, potentially affecting human lipid metabolism and health. This study expunge shed light on the ecological toxicity of spirotetramat by showing how it disrupts lipid metabolism and causes tissue damage specifically in zebrafish liver, contributing to a deeper understanding of its harmful effects in aquatic environment.

Toxic Effects of Carbaryl Exposure on Juvenile Asian Seabass (Lates calcarifer).

This study examines the physiological and immunological effects of 0.5 ppm carbaryl exposure on juvenile Asian seabass (Lates calcarifer) over 12 h to 72 h. Notable results include decreased activities of liver enzymes catalase (CAT), lactate dehydrogenase (LDH), and glutathione peroxidase (GSH-PX), while superoxide dismutase (SOD) levels remained stable, with the lowest activities of CAT and GSH-PX observed at 72 h. Serum biochemistry revealed increased alkaline phosphatase (AKP) and acid phosphatase (ACP) at 24 h, with declining aspartate aminotransferase (AST) and a peak in creatinine at 48 h. Histopathological analysis showed carbaryl-induced necrosis in liver and spleen cells, and increased melanomacrophage centers in both organs. Additionally, immune gene expression analysis indicated an upregulation of heat shock proteins and consistent elevation of complement component C3 and interleukin-8 (IL-8). These findings suggest that carbaryl exposure significantly impairs organ function and modulates immune responses in L. calcarifer, underlining the need for further research on protective strategies against pesticide impacts in aquaculture.

Assessing the Impact of Pomegranate Juice on Liver Tissue in Male Rats Exposed to a Commercial Energy Drink

The current study was designed to investigate the effect of pomegranate juice on some biochemical and histological variables resulting from dosing male rats with the energy drink Red Bull. In this study, 28 white male rats were used, divided into four groups, each involving seven animals, according to the following: G1 was given a physiological solution (5 ml/kg) and a standard diet for 120 days; G2 was given a dose of the energy drink Red Bull (volume 1 ml per 100 g); G3 was given pomegranate juice (5 ml/kg) first; then Red Bull; and G4 was given Red Bull first; and after six weeks, he was given pomegranate juice. The results showed that Red Bull consumption significantly elevated RBS, AST, ALT, TC, and TG levels. Pomegranate juice has the ability to reduce the concentration of RBS, AST, ALT, TC, and TG. Histological changes in the liver of animals that were given the Red Bull energy drink were represented by congestion of the central vein, degeneration, and necrosis of liver cells, with severe infiltration of inflammatory cells and a thick wall of the central vein (TW), as well as amyloid (AM) deposition, compared to the negative control group. The results of the histological examination showed that pomegranate juice could repair cellular tissue in the liver and make it similar to the tissue of a control normal group, denoting the possibility of using it in the diet and in treating atherosclerosis and heart disease. Keywords: Pomegranate juice, liver, rats, energy drink, rat model, atherosclerosis, heart disease.

Preliminary study on the diagnostic value of LEAP-2 and CK18 in biopsy-proven MAFLD

Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) has become the leading cause of chronic liver disease. Liver biopsy, as the diagnostic gold standard, is invasive and has sampling bias, making it particularly important to search for sensitive and specific biomarkers for diagnosis. Cytokeratin 18 (CK18) M30 and M65 are products of liver cell apoptosis and necrosis, respectively, and liver-expressed antimicrobial peptide 2 (LEAP-2) is a related indicator of glucose and lipid metabolism. Correlation studies have found that all three indicators positively correlate with the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Through comparison of diagnostic values, it was found that CK18 M65 can better distinguish between healthy individuals and MAFLD; LEAP-2 can effectively distinguish MAFLD from other liver diseases, especially ALD.

MicroRNA‐Modified DNA Hexahedron‐Induced Hepatocyte‐Like Cells Integrating 3D Printed Scaffold for Acute Liver Failure Therapy

AbstractAcute liver failure (ALF) involves extensive necrosis of liver cells and severe impairment of liver function. Hepatocyte transplantation holds promise for treating ALF by swiftly supporting liver functions and promoting liver regeneration. However, the scarcity of suitable cell sources requires strategies to obtain enough functional hepatocyte‐like cells (HLCs) and optimize their in vivo transplantation efficiency. A DNA hexahedral nanostructure (DHN) is developed loaded with microRNA‐122 to efficiently induce hepatic differentiation of human adipose‐derived mesenchymal stem cells into HLCs. These HLCs can serve as alternative hepatocyte sources, as confirmed by expression of liver‐specific genes and proteins, and the restoration of liver functions. To enhance in vivo survival efficiency of HLCs, a versatile scaffold is also created by 3D printing the calcium‐cross‐linked mixture bioink composed of sodium alginate, gelatin, and silk fibroin with excellent ROS scavenging capabilities. The scaffold is infused with chitosan‐DHN hydrogel containing HLCs for tissue engineering orthotopic transplantation in CCl4‐induced ALF mice. The transplanted composite scaffold‐HLCs successfully repair tissue necrosis in the liver injury area of mice and regulate expressions of genes and proteins associated with inflammation, oxidative stress, and hepatocyte function. Collectively, this study offers a novel approach and strategy for identifying alternative hepatocyte sources and treating ALF.

The effect of bisphenol A on antioxidant defense and the structure and function of the liver of Siberian sturgeon (Acipenser baerii).

The present study was conducted to investigate the biochemical and histological changes of liver tissue in Siberian sturgeon (Acipenser baerii) exposed to different doses of bisphenol A (BPA). One hundred and eighty pieces of 1-year-old A. baerii with an average weight of 200-250 g bought and randomly distributed in 18 tanks (n = 10). After 2 weeks of adaptation, the fish received intraperitoneal injections of 1, 10, and 100 μg/g/week BPA and μg/g/week of 17β-estradiol intraperitoneally. The solvent control group received only peanut oil, while the control group did not receive any injections. In order to investigate histological changes of the liver, after 2 weeks the liver samples were taken, fixed in 10% formalin solution and slides prepared by routine histological methods. For assaying antioxidant defense status, the liver tissue from three fish of each replicates was captured and after homogenization, activity of catalase, superoxide dismutase, and glutathione peroxidase and malondialdehyde measured. The most important histological changes observed in the liver tissue were: vacuolation of hepatocytes, nuclear hypertrophy, necrosis of liver cells, expansion of sinusoids, and accumulation of fat cells. In the highest dose, the intensity of tissue changes increased. Activity of antioxidant enzymes and malondialdehyde content increased in fish exposed to 100 μg/g/week BPA in compare with other groups (p < .05). According to our findings, it could be concluded that liver histology was affected by BPA and tissue damage had occurred, which had led to changes in blood parameters. Also, the obtained results showed that the high concentrations of BPA used in this study stimulate the antioxidant defense. RESEARCH HIGHLIGHTS: BPA evoke oxidative stress in Siberian sturgeons in high dose of exposure. Severity of liver histologic lesions was dose dependent.

Hypolipidemic and hepatoprotective effects of corn silk extract in nicotine-administered male mice.

This study is done to investigate the hypolipidemic and hepatoprotective effects of corn silk extract in nicotine-administered male mice. Nicotine can induce pathophysiological effects in the liver tissue through oxidative stress and damage cells. Corn silk can improve liver function with its antioxidant effects. In this experimental study, 30 male NMRI mice (25-30 gr) were divided into 5 groups: controls, sham, nicotine 2.5 mg/kg, nicotine+aqueous extract of corn silk 400 mg/kg, and nicotine+methanolic extract of corn silk 400 mg/kg for 1 month. One day after the last nicotine and extracts consumption, the serum samples were performed for biochemical measurement, and the supernatant of the homogenized liver was administered for antioxidant variables assessment. There was no significant difference in the body weight of different groups. Liver weight and GSH decreased in the nicotine group compared to the control group (P<0.05). Triglycerides, total cholesterol, HDL-C, LDL-C, liver enzymes, and MDA increased in the nicotine group compared to the control group (P<0.05). Also, the expansion of sinusoids, the presence of inflammatory cells, and necrosis of liver cells were observed in the nicotine group compared to the control group. Using aqueous and methanolic extracts of corn silk in mice receiving nicotine led to the improvement of the mentioned variables (P<0.05). The results of this study showed that the use of nicotine can lead to the induction of hepatotoxicity. The use of aqueous and methanolic extracts of corn silk improved them through its antioxidant activity.

Hepatic Cirrhosis and its Management via Electro-Homoeopathic Practices

Hepatic cirrhosis is known by the development of regenerative nodules in liver parenchyma surrounded by fibrous septa resultant to chronic liver damage. Cirrhosis happens due to necrosis of liver cells followed by fibrosis and nodule formation. The liver organization come to be abnormal and interferes with liver blood flow and function, and eventually pointers to portal hypertension followed by hepatocytic dysfunction. Chronic liver diseases signify a remarkable health problem across the world with liver cirrhosis. The exact prevalence of cirrhosis worldwide was ambiguous due to the clinical continuum ranging from apathetic, asymptomatic to whole liver decompensation. Therefore, recurrent inputs via a series of research in view of various conventional and definite earlier techniques in background, along this thrust medical area, directed an emerging and medically most precise an alternate technique, namely, Electro-Homoeopathic Medical Science that has been presently in practice by a number of practitioners in India and southeast Asian countries enlightening attractive outcome without any significant post therapeutic physiological and/or biochemical side effect concomitant with risk factor. Various clinical practices and survey provide new insights into the development and establishment of an increasingly advanced form of the electro-homeopathic system for a defined diagnosis enlightening a definite root cause and efficient management of Liver Disease as well as its perception.

Visualization of therapeutic intervention for acute liver injury using low-intensity pulsed ultrasound-responsive phase variant nanoparticles.

Acute liver injury (ALI) is a highly fatal condition characterized by sudden massive necrosis of liver cells, inflammation, and impaired coagulation function. Currently, the primary clinical approach for managing ALI involves symptom management based on the underlying causes. The association between excessive reactive oxygen species originating from macrophages and acute liver injury is noteworthy. Therefore, we designed a novel nanoscale phase variant contrast agent, denoted as PFP@CeO2@Lips, which effectively scavenges reactive oxygen species, and enables visualization through low intensity pulsed ultrasound activation. The efficacy of the nanoparticles in scavenging excess reactive oxygen species from RAW264.7 and protective AML12 cells has been demonstrated through in vitro and in vivo experiments. Additionally, these nanoparticles have shown a protective effect against LPS/D-GalN attack in C57BL/6J mice. Furthermore, when exposed to LIPUS irritation, the nanoparticles undergo liquid-gas phase transition and enable ultrasound imaging.

Catapol attenuates the aseptic inflammatory response to hepatic I/R injury in vivo and in vitro by inhibiting the HMGB1/TLR-4/NF-κB signaling pathway via the microRNA-410–3p

BackgroundHepatic ischemia-reperfusion (I/R) injury involves inflammatory necrosis of liver cells as a significant pathological mechanism. Catapol possesses anti-inflammatory activity that is extracted from the traditional Chinese medicine, Rehmannia glutinosa. MethodsThe liver function and histopathology, Oxidative stress, and aseptic inflammatory responses were assessed in vivo, and the strongest dose group was selected. For mechanism, the expression of miR-410–3p, HMGB1, and TLR-4/NF-κB signaling pathways was detected. The dual luciferase assay can verify the targeting relationship between miR-410–3p and HMGB1. Knockdown of miR-410–3p in L02 cells is applied in interference experiments. ResultsCAT pre-treatment significantly decreased the liver function markers alanine and aspartate aminotransferases and reduced the areas of hemorrhage and necrosis induced by hepatic I/R injury. Additionally, it reduced the aseptic inflammatory response and oxidative stress, with the strongest protective effect observed in the high-dose CAT group. Mechanistically, CAT downregulates HMGB1, inhibits TLR-4/NF-κB signaling pathway activation, and reduces inflammatory cytokines TNF-α, and IL-1β. In addition, the I/R-induced downregulation of microRNA-410–3p was inhibited by CAT pre-treatment in vivo and in vitro. HMGB1 was identified as a potential target of microRNA-410–3p using a dual-luciferase reporter assay. Knockdown of microRNA-410–3p abolished the inhibitory effect of CAT on HMGB1, p-NF-κB, and p-IκB-α protein expression. ConclusionsOur study showed that CAT pre-treatment has a protective effect against hepatic I/R injury in rats. Specifically, CAT attenuates the aseptic inflammatory response to hepatic I/R injury in vivo and in vitro by inhibiting the HMGB1/TLR-4/NF-κB signaling pathway via the microRNA-410–3p.

Synergistic effect rescue animal model from NASH caused by diet-inflammation inducer

Excessive intake of pro-inflammatory fatty acids is related to the development of insulin resistance, impaired oxidative stress enzymes, and lipid disorders, leading to inflammation and development of non-alcoholic steatohepatitis (NASH). Diet and physical exercise are considered to prevent and treat metabolic disorders caused by chronic inflammatory states (responsible for insulin resistance and diabetes type 2) in individuals with obesity and nonalcoholic fatty liver diseases (NAFLD). Our investigation tested the hypothesis that Hass avocado oil, a monounsaturated fatty acid and a source of phytosterol, may improve liver and metabolic parameters without adverse effects when combined with physical exercise. Rats ingested a high-fat diet for seven weeks and were then subjected to more six weeks with a standard diet, Hass avocado-oil ingestion, and swimming. The intervention showed significantly improvements by synergistic effect between Hass avocado-oil and swimming exercise (P < 0.05), including improving adiponectin, leptin, and fasting blood glucose levels, alleviating insulin resistance, reducing serum TNF-α, improving glutathione enzyme levels, and decreasing lipotoxicity in the liver and blood and serum triacylglycerides in blood (P < 0.05). Liver tissue markers of apoptosis and necrosis such as CK-18 filaments and dimethylamine (DMA) were significantly higher in the intervention group (P < 0.05). We were unable to fully confirm our hypothesis. Although the synergistic effects between Hass avocado-oil and the swimming regimen offer a promising chance of recovering liver health by improving 10 health biological markers, we must not ignore the cellular damage due to apoptosis and necrosis in liver cells and DMA. The data on metabolomic profile and avocado-oil-treated livers highlight the need for further investigation.

Aflatoksin: Aspek kesehatan, metode reduksi dan deteksinya

Food contaminant aflatoxin is a mycotoxin produced by Aspergillus flavus and A. parasiticus. This article aims to discover the pathophysiological, immunological, pharmacological, toxicity, and reduction and detection methods of aflatoxin. Kinds of literature were obtained from Research Gate, Pubmed, and Science Direct with the primary keyword “aflatoxin”. Pathophysiologically, aflatoxin-contaminated food has been proven to cause necrosis in liver cells, developing into liver cancer. Immunologically, aflatoxin decreases monocyte and dendritic cell phagocytosis, neutrophil cell ATP production, and pro-inflammatory cytokine synthesis. Aflatoxin toxicity is at the LD50 of 12-16 mg/kg b.w, causing death. Pharmacologically, 120-201 µg/kg b.w causes aflatoxicosis, in vivo studies indicated that NovaSil, Sulfarophan, and Monanthotaxis caffra leaf extract may reduce its toxicity. Aflatoxins are highly thermostable; hence, once food has been contaminated, they cannot be destroyed by normal cooking process. The control and reduction should be conducted in post-harvest handling, common physical means practiced are heating, drying, and smoking. Chemically using ozone, 0.5 sodium bisulfate, 1% sodium hydroxide, 5% acetic acid, and prochloraz. Biologically using Flavobacterium aurantiacum B-184, Bacillus velezensis DY3108, and, a consortium of Geobacillus and Tepidimicrobium bacteria. Aflatoxin can be detected using TLC, HPLC, MS, ELISA, and UHPLC-ESI MS/MS. The prevention of aflatoxin occurrence is done through good post-harvest handling, good manufacturing practices, and applying regulations accordingly to ensure food products and feed are at acceptable levels of aflatoxin.

English

Poultry oil is commonly used as a cost-effective energy source in poultry feed. However, when used at higher levels, raw poultry oil has been found to have adverse effects on the liver of birds. Unfortunately, many poultry farmers remain unaware of these harmful effects. The objective of this experiment was to investigate how poultry oil impacts liver health and contributes to fatty liver syndrome in layers. Using a completely randomized design, 120 Lohmann Single Comb (LSL-Lite) layers (25- week-old) were randomly assigned to 4 experimental groups, each of which had 30 birds. Increasing amounts of poultry oil (0, 1.5, 3.0 and 4.5%) were used in experimental diets. Hens were fed these experimental diets for 20 weeks. The results showed maximum liver fat percentage in 4.5% poultry oil in diet, severe liver congestion, degeneration and cell necrosis in caged layers. Plasma lipid profile (cholesterol, HDL, LDL, triglycerides) and liver enzymes (AST, ALT, ALP and LDH) were significantly (p&lt;0.05) affected by poultry oil addition. Higher liver scores indicative of fatty liver syndrome was observed in layers receiving 4.5% poultry oil, while the control group showed the lowest incidence. This study indicated that poultry oil dietary addition at a higher level (4.5%) lead to an increased serum lipid profile and has a negative impact on liver health, ultimately causing fatty liver syndrome in caged layers

Vitamin D3 activates the innate immune response and xenophagy against Nocardia seriolae through the VD receptor in liver of largemouth bass (Micropterus salmoides)

Nocardia seriolae is a pathogenic bacterium that commonly infects largemouth bass (Micropterus salmoides), causing chronic wasting disease characterized by multiple nodules. The mechanism by which Vitamin D3 (VD3) can resist Nocardia seriolae (N. seriolae)infection is unknown, although VD3 has been found to regulate innate immune response and xenophagy in mammals. Therefore, we investigated the effects of VD3 on the immune response and xenophagy of largemouth bass after N. seriolae challenge. The results demonstrate that increasing dietary VD3 intake can alleviate focal necrosis of liver cells, increase mRNA and protein levels of innate immune response-related genes, such as cGAS, STING1, TBK1, IRF3, and IFNα, decrease the content of liver autophagosomes, and increase the content of liver autophagolysosomes. Additionally, VD3 can increase mRNA expression and protein levels of genes related to liver autophagosome-lysosome fusion, including ATG16L1, ATPV0Ca, ATPV0Cb, ATPV1D, LAMP2, STX17, and VAMP8, as well as VDR. These findings suggest that VD3 contributes to the resistance of largemouth bass to N. seriolae infection by activating innate immune response and xenophagy through VDR-mediated immunomodulation.

Research progress of extracellular vesicles and exosomes derived from mesenchymal stem cells in the treatment of oxidative stress-related diseases.

There is growing evidence that mesenchymal stem cell-derived extracellular vesicles and exosomes can significantly improve the curative effect of oxidative stress-related diseases. Mesenchymal stem cell extracellular vesicles and exosomes (MSC-EVs and MSC-Exos) are rich in bioactive molecules and have many biological regulatory functions. In this review, we describe how MSC-EVs and MSC-Exos reduce the related markers of oxidative stress and inflammation in various systemic diseases, and the molecular mechanism of MSC-EVs and MSC-Exos in treating apoptosis and vascular injury induced by oxidative stress. The results of a large number of experimental studies have shown that both local and systemic administration can effectively inhibit the oxidative stress response in diseases and promote the survival and regeneration of damaged parenchymal cells. The mRNA and miRNAs in MSC-EVs and MSC-Exos are the most important bioactive molecules in disease treatment, which can inhibit the apoptosis, necrosis and oxidative stress of lung, heart, kidney, liver, bone, skin and other cells, and promote their survive and regenerate.

Isolation, Identification, and Whole Genome Analysis of Chicken Infectious Anemia Virus in an Outbreak of Disease in Adult Layer Hens.

Chicken infectious anemia (CIA) poses a significant threat to the chicken industry in China. Due to its non-specific symptoms, the disease is often overlooked. This study aimed to conduct a comprehensive analysis of the etiology and pathology of CIA in Guangxi Province, China. Three strains of the chicken infectious anemia virus (CIAV) were isolated from liver samples of diseased 20-week-old chickens. The complete genomes of these strains were sequenced, and experiments on specific pathogen-free (SPF) chicks revealed that the GX21121 strain exhibited high virulence. Histopathological examination of the deceased chickens showed liver cell necrosis, fibrous serous exudation, inflammatory cell infiltration, hemorrhage in liver tissues, and congestion in lung and renal tissues. Phylogenetic analysis of the genome revealed that the three strains had a close genetic relationship to the Heilongjiang wild-type strain (GenBank KY486144). The genetic evolution of their VP1 genes indicated that all three CIAV isolates belonged to genotype IIIc. In summary, this study demonstrated the genomic diversity of three CIAV strains in adult layer hens. The isolation and characterization of the GX21121 strain as a highly virulent isolate provide valuable information for further investigations into the etiology, molecular epidemiology, and viral evolution of CIAV.

Effect of Some Medicinal Plants Extracts and Chemicals on Enzymes and Tissues Liver of Female Rats

The study was carried out on 45 sexually mature female albino rats at the age of 7-8 weeks and weighing 160-180; nine treatments were used in this study, where five rats were isolated for the control treatment (without infection); the remaining rats were injected (Subcutaneous) with Indian-made Alloxan, which was prepared at the time of injection at a dose of 100 mg/kg of body weight. The results showed a significant decrease in liver enzymes AST and the ALP characteristic in T3, T4, T5, T6, T7, T8, and T9, as well as a significant decrease in the ALT characteristic in T3, T5, T6, T7, and T9. Histological effects We notice severe damage to the liver tissue of alloxan-treated rats compared to the proper treatment, represented in the liver tissue by necrosis of liver cells, the presence of a blood clot, the absence of sinusoids, and the thickening of the nuclei. The results have shown that the aqueous extracts positively affect zymes and tissues in female rats.

Liver abscess caused by Clostridium perfringens after left hepatic trisectionectomy for perihilar cholangiocarcinoma: a case report

BackgroundClostridium perfringens sepsis has been reported to have a rapid onset and severe clinical outcome. We herein report a case of C. perfringens sepsis associated with massive intravascular hemolysis after left hepatic trisectionectomy for perihilar cholangiocarcinoma.Case presentationA 72-year-old woman underwent left hepatic trisectionectomy for perihilar cholangiocarcinoma. Her postoperative course was uneventful except for bile leakage. She was discharged on postoperative day (POD) 35. On POD 54, she was readmitted because of abdominal pain with a high fever. Although her vital signs were stable on arrival at the hospital, a laboratory examination showed a severe inflammatory reaction and hemolysis, and she had developed disseminated intravascular coagulation. Abdominal contrast-enhanced computed tomography showed a 70-mm irregular shape and low-density containing air in liver segment 6, which suggested a liver abscess. The abscess was immediately drained of pus containing air. The pus showed multiple Gram-positive bacilli, and two blood cultures showed Gram-positive bacilli and hemolysis. Empirical antibiotic therapy with vancomycin and meropenem was started because C. perfringens was detected from the preoperative bile culture. Four hours after arrival, tachypnea and decreased oxygen saturation were observed. Her general condition deteriorated rapidly with significant hypoglycemia, progressive acidosis, anemia, and thrombocytopenia. Despite rapid drainage and empiric therapy, she died six hours after her arrival. At autopsy, the abscess consisted of coagulation necrosis of liver cells with inflammatory cell infiltration, and clusters of Gram-positive large bacilli were observed in the necrotic debris. C. perfringens was detected in the drainage fluid and blood culture. She was diagnosed with a liver abscess and severe sepsis caused by C. perfringens and treated promptly, but the disease progressed rapidly and led to her death.ConclusionsSepsis caused by C. perfringens can progress rapidly and lead to death in a few hours, so prompt treatment is needed. When patients who have undergone highly invasive hepatobiliary-pancreatic surgery show hemolysis and hepatic abscesses with gas, C. perfringens should be considered the most likely bacterium.

Green Synthesis, Characterization, and Antiparasitic Effects of Gold Nanoparticles against Echinococcus granulosus Protoscoleces.

Echinococcosis, or hydatidosis, is one of the most important zoonotic diseases, which is initiated by the larval stage in the clasts of Echinococcus granulosus. For the treatment of hydatidosis, surgery is still the preferred method and the first line of treatment for symptomatic patients. Unfortunately, most of the scolicidal agents that are injected inside cysts during hydatid cyst surgery have side effects, including leaking out of the cyst and adverse effects on the living tissue of the host, such as necrosis of liver cells, which limits their use. This work was carried out to study the lethal effect of green synthesized gold nanoparticles (Au-NCs) against hydatid cyst protoscoleces. Au-NCs were green synthesized using the Saturja khuzestanica extract. Au-NCs were characterized by UV-visible absorbance assay, electron microscopy analysis, X-ray diffraction (XRD), and Fourier transform infrared (FTIR) spectroscopy. Scolicidal properties of Au-NCs (1-5 mg/mL) were studied against protoscoleces for 10-60 min. The effect of Au-NCs on the expression level of the caspase-3 gene as well as the ultrastructural examination was studied by real-time PCR and scanning electron microscopy (SEM). The cytotoxicity of Au-NCs on hepatocellular carcinoma (HepG2) and normal embryonic kidney (HEK293) cell lines was also studied by the cell viability assay. The obtained Au-NCs are cubes and have an average size of 20-30 nm. The highest scolicidal efficacy was observed at 5 mg/mL with 100% mortality after 20 min of treatment for hydatid cyst protoscoleces. In ex vivo, Au-NCs required more incubation time, indicating more protoscolicidal effects. Au-NCs markedly upregulated the gene level of caspase-3 in protoscoleces; whereas they changed the ultra-structure of protoscoleces by weakening and disintegrating the cell wall, wrinkles, and protrusions due to the formation of blebs. We showed the effective in vitro and ex vivo scolicidal effects of Au-NCs against hydatid cyst protoscoleces by provoking the apoptosis process of caspase-3 activation and changing the ultrastructure of protoscoleces with no significant cytotoxicity against human normal cells. However, additional studies should be conducted to determine the possible harmful side effects and accurate efficacy.