Serum Levels Of Enzymes Research Articles

Downregulation of proinflammatory cytokines and dynamic expression of TGF-β1 molecules induced by anti-IL-17 mAb in murine schistosomiasis mansoni

Hepato-intestinal schistosomiasis is characterized by severe pathological changes at advanced chronic stages, including granulomatous lesions and liver fibrosis. The objective of our research was to assess the dynamic expression of profibrotic molecules, the transforming growth factor beta 1 (TGF-β1), and proinflammatory cytokines immunomodulation induced by interleukin 17 (IL-17) neutralization in murine Schistosomiasis mansoni. The study included 56 specific pathogen-free male C57BL/6 mice, divided into 3 main groups: GI uninfected normal controls, GII S. mansoni infected with 70±5 cercariae/non-treated, GIII S. mansoni infected and treated with anti-IL-17 monoclonal antibody (mAb), GIV S. mansoni infected and isotype-matched IgG2a mAb was given as a challenge. Mice were sacrificed at 6, 8, and 10 weeks after infection, then their liver enzymes and cytokines assessed, histopathological and immunohistochemical tested. The present study demonstrated a statistically significant elevation in serum levels of IL-17 (p<0.01), TGF-β1 (p<0.01), IL-1β (p≤0.001), IL-4 (p≤0.003), IL-6 (p≤0.05), and liver enzymes (ALT: p≤0.001; AST: p≤0.002). Additionally, granulomatous lesions and TGF-β1 expression were significantly increased (p<0.001) in infected mice at 6, 8, and 10 weeks after infection. All showed significant reduction by neutralization with anti-IL-17 mAb. Finally, IL-17 exhibited potent profibrogenic activity, and anti-IL-17 mAb can be used to alleviate and counteract this impact in murine S. mansoni.

Zinc pretreatment for protection against intestinal ischemia-reperfusion injury.

Intestinal ischemia-reperfusion (I/R) injury (II/RI) is a critical condition that results in oxidative stress, inflammation, and damage to multiple organs. Zinc, an essential trace element, offers protective benefits in several tissues during I/R injury, but its effects on intestinal II/RI remain unclear. To investigate the effects of zinc pretreatment on II/RI and associated multiorgan damage. C57BL/6 mice were pretreated with zinc sulfate (ZnSO4, 10 mg/kg) daily for three days before I/R injury was induced via superior mesenteric artery occlusion (SMAO) and abdominal aortic occlusion (AAO) models. Tissue and serum samples were collected to evaluate intestinal, liver, and kidney damage using Chiu's score, Suzuki score, and histopathological analysis. Caco-2 cells and intestinal organoids were used for in vitro hypoxia-reoxygenation injury models to measure reactive oxygen species (ROS) and superoxide dismutase (SOD) levels. Zinc pretreatment significantly reduced intestinal damage in the SMAO and AAO models (P < 0.001). The serum levels of liver enzymes (alanine aminotransferase, aspartate aminotransferase) and kidney markers (creatinine and urea) were lower in the zinc-treated mice than in the control mice, indicating reduced hepatic and renal injury. In vitro, zinc decreased ROS levels and increased SOD activity in Caco-2 cells subject to hypoxia-reoxygenation injury. Intestinal organoids pretreated with zinc exhibited enhanced resilience to hypoxic injury compared to controls. Zinc pretreatment mitigates II/RI and reduces associated multiorgan damage. These findings suggest that zinc has potential clinical applications in protecting against I/R injuries.

Correlation Between Lipid Profile and Liver Function in Patients With Non-Alcoholic Fatty Liver

Background: Non-alcoholic fatty liver disease (NAFLD) is a metabolic liver disease characterized by a broad range of liver pathology, including simple steatosis, steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocarcinoma. NAFLD has emerged as a public health concern in the world within the last 20 years, it is linked to metabolic syndrome (MetS), type 2 diabetes mellitus (T2DM), obesity, and dyslipidemia. Increased visceral adipose tissue in obese people can cause insulin resistance (IR) and hyperinsulinemia, which will speed up the lipolysis of adipose tissue, Lipo-toxicity-related chronic low-grade inflammation is involved in the development of NAFLD. Objective: Determine the correlation between lipid profile and liver function in patients with NAFLD. Patients and Methods: A study was conducted at Tikrit Teaching Hospital from 28 November to 28 December 2023. The study involved 90 participants, 60 with NAFLD and 30 healthy subjects. The study used a spectrophotometer (Model NO. HV-2800EX) and a colorimetric kit from Spain linear chemicals to determine various parameters, such as Aspartate aminotransferase (AST), Alanine aminotransferase(ALT), Gamma-glutamyl transferase(GGT), High-density lipoprotein(HDL), Low-density lipoprotein(LDL), Very low-density lipoprotein(VLDL), Triglyceride(TG), and cholesterol. Results: The mean age of patients in the group was 40.93 years, with ages ranging from 20 to 50 years. Serum levels of liver function enzymes (GGT, AST, ALT) and lipid profile (TG, HDL, LDL, VLDL, cholesterol) were measured and compared to the control groups. Patients with NAFLD had significantly higher serum liver function enzymes and increased serum lipid profile (TG, VLDL, LDL, and cholesterol) while showing a significant decrease in HDL concentration when compared to the control group. Conclusion: The patients showed an increase in liver function enzymes (AST, ALT, GGT) and lipid profile (LDL, VLDL, TG, cholesterol) with reduced HDL as compared to healthy individuals. Keywords: Nonalcoholic fatty liver, liver function enzymes, lipid profile.

Coleus vettiveroides Root Extract Protects Against Thioacetamide-Induced Chronic Liver Injury by Inhibiting NF-κB Signaling Pathway.

The roots of Coleus vettiveroides (CV) have been traditionally used in Indian medicinal systems such as Ayurveda and Siddha for its antioxidant, anti-inflammatory, and antidiabetic effects. This study examines the antifibrotic potential of CV ethanolic root extract (CVERE) against thioacetamide (TAA)-induced liver fibrosis in Wistar rats. TAA was administered via i.p., thrice weekly for 11 weeks to induce liver fibrosis in rats. In separate groups, rats were administered with TAA and were concurrently treated with CVERE 125 mg/kg, CVERE 250 mg/kg, and silymarin (SIL) 100 mg/kg. Liver marker enzymes of hepatotoxicity, oxidative stress markers, proinflammatory marker gene expression (TNF-α, NF-κB, COX, and ILs), fibrotic marker gene expression (collagen I and III), immune histochemical expression of fibrosis marker proteins, and histopathologic changes were analyzed. TAA administration led to a significant (p < 0.001) increase in the serum level of hepatotoxic marker enzymes. The TAA-treated group showed higher levels (p < 0.001) of MDA and reduced activities of SOD and CAT in the liver. TAA administration increased CYP2E1 expression, proinflammatory, and fibrotic marker gene expressions in rat liver. The histopathology of the liver confirms TAA-induced architectural distortion and fibrotic changes. CVERE and SIL simultaneous treatments significantly protected against TAA-induced oxidative stress, inflammation, and liver fibrosis. In conclusion, CVERE inhibited TAA-induced liver fibrosis through downregulation of TAA metabolic activation, redox imbalance, and inflammation through repression of the NF-κB pathway.

Protective effects of Pelargonium graveolens (geranium) oil against cefotaxime-induced hepato-renal toxicity in rats.

Cefotaxime is a broad-spectrum antibiotic targeting Gram-negative bacteria used for diverse infections, but it can be toxic to the stomach, liver, and kidneys. This study explored the protective effects of geranium oil against cefotaxime-induced hepatotoxicity and nephrotoxicity in rats, employing biochemical, histopathological, and immunohistochemical evaluations. Thirty rats were divided into five groups of six animals each one. Group 1 received orally normal saline for 14days, Group 2 was given orally 2.5% DMSO for 14days, Group 3 received cefotaxime (200mg/kg/day IM) for 14days, Group 4 received with cefotaxime (200mg/kg/day IM) and geranium oil (67mg/kg b. w./day orally in DMSO) for 14days, and Group 5 received geranium oil alone (67mg/kg b. w./day orally in DMSO) for 14days. Geranium oil significantly reduced cefotaxime-induced damage, evidenced by lower serum levels of liver enzymes (AST, ALT), renal markers (urea, creatinine), and other indicators (alkaline phosphatase, TNF-alpha, IL-1Beta, MAPK, nitric oxide, MDA). It also increased levels of protective tissue biomarkers such as NrF2, albumin, catalase, Beclin 1, and reduced glutathione (GSH). Histopathological and immunohistochemical analyses revealed significant protective effects in liver and renal tissues in rats treated with Geranium oil. These results suggest that Geranium oil is effective in mitigating cefotaxime-induced hepatotoxicity and renal toxicity.

Assessment of serum levels of nutrients and liver enzymes during early lactation in crossbred dairy cattle

Assessment of serum levels of nutrients and liver enzymes during early lactation in crossbred dairy cattle

Biochemical Investigation of the Association of Apolipoprotein E Gene Allele Variations with Insulin Resistance and Amyloid-β Aggregation in Cardiovascular Disease.

This article investigates the intricate associations between apolipoprotein E (APOE) gene alleles variation, insulin resistance (IR) and amyloid-β aggregation in cardiovascular disease (CVD) patients. A cohort of 250 patients exhibiting the symptoms of CVD and 50 control subjects participated in this study. After applying the stringent inclusion and exclusion criteria, the diseased group was further stratified into three categories: CVD+ (Alzheimer's disease) AD, CVD + (diabetes mellitus) DM and CVD + DM + AD. Blood samples were collected from all recruited participants for the biochemical analyses of lipid profile, glycaemic status, liver function enzymes, inflammatory and oxidative stress biomarkers. Tetra amplification-refractory mutation system-polymerase chain reaction (ARMS-PCR) was employed for APOE gene analysis. Biochemical evaluations revealed the significant elevations in the serum levels of glucose, liver enzymes, interleukin-6 (IL-6), cholesterol, low-density lipoproteins (LDL), triglycerides (TG) and malondialdehyde (MDA) in CVD + DM + AD group. Conversely, the serum levels of insulin, HDL and hexokinase decreased in CVD + DM + AD group compared to the controls and other CVD groups. Tetra ARMS-PCR results indicated a higher percentage of the risk allele in CVD + DM + AD group when compared with the other groups. Our study elucidates the multifaceted cardiovascular risk factors contributing to IR and AD in CVD patients. Age-related risk factors, prevalence of APOE risk alleles and the impact of statin use on AD incidences were identified. These findings underscore the need for tailored preventive measures, particularly in APOEε4 and ε3/ε4 carriers with CVD. Further studies should delve into the knowledge-based protocols to comprehend the underlying mechanisms. Focusing on the therapeutic targets to prevent or delay DM and AD progression in CVDs, especially in APOEε4 carriers, is essential.

Sildenafil and Vitamin E Alone or in Combination Suppresses Cyclophosphamide-Induced Hepatotoxicity in Rats Through Antioxidant Mechanisms

Background: Cyclophosphamide (CP) can induce severe hepatotoxicity in certain patients by generating oxidative molecules and increasing reactive oxygen species (ROS). There are limited reports on the antioxidant and anti-inflammatory properties of Sildenafil. Objectives: This study aimed to evaluate the effect of Sildenafil on CP-induced hepatotoxicity. Methods: Animals were randomly divided into five groups (n = 6): Group I (control) received water distillate by gavage. Group II received CP (200 mg/kg) intraperitoneally to induce hepatotoxicity. Group III was orally administered Sildenafil (75 mg/kg) along with CP (200 mg/kg), while Group IV received vitamin E (500 mg/kg) and CP (200 mg/kg). Group V was administered 75 mg/kg of Sildenafil, 200 mg/kg of CP, and 500 mg/kg of vitamin E. At the end of the experiment, blood samples were collected from the animals' hearts to measure serum levels of liver enzymes, including aspartate transaminase (AST) and alanine aminotransferase (ALT), as well as oxidative stress markers malondialdehyde (MDA), nitric oxide (NO), and ferric reducing antioxidant power (FRAP). Liver tissue was also collected for assessment of antioxidant enzyme activity, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), along with histological examination. Results: The CP-treated group exhibited significant increases in AST, ALT, MDA, and NO levels, while CAT, SOD, GPx, and FRAP levels were markedly lower in the CP group compared to the saline group (P ≤ 0.01). Administration of sildenafil, alone and in combination with vitamin E, significantly reduced levels of AST, ALT, MDA, and NO. Meanwhile, antioxidant enzyme activity was markedly enhanced following sildenafil and vitamin E intake (P ≤ 0.01). Additionally, histological analysis confirmed Sildenafil's hepatoprotective properties. Conclusions: This study demonstrated that Sildenafil, both alone and in combination with vitamin E, was effective in reducing CP-induced liver toxicity through antioxidant mechanisms. Therefore, these findings suggest that Sildenafil, especially when combined with vitamin E, may serve as a complementary therapy to mitigate the hepatotoxic effects of CP.

Isatin-1,2,3-triazole derivatives: Synthesis, molecular docking and evaluation against acute experimental toxoplasmosis

Toxoplasmosis remains a challenge for both public health and animal husbandry which created a constant demand to develop novel compounds using innovative methods. To join this relentless quest for an ideal chemotherapeutic agent, herein, we developed newly synthesized isatin-1,2,3-triazole derivatives. Three compounds (5a, 5b and 5c) were synthesized, characterized, loaded on chitosan nanoparticles (CNPs) and then evaluated accordingly. Initially, a molecular docking study was carried out which revealed the effective interaction with the target enzymes; purine nucleoside phosphorylase (PNPase) and T. gondii calcium-dependent protein kinase-1 (TgCDPK1). This was further substantiated by in vivo evaluation of the three compounds (5a-c) and their nanoformulae (5a-CNPs, 5b-CNPs, and 5c-CNPs) against acute Toxoplasma gondii infection in murine model. It is worthy of note that all tested compounds and their nanoformulae produced a statistically significant reduction of parasite burden in both peritoneal fluid and liver impression smear and profound ultrastructural alterations, detected by scanning electron microscopy, compared to the infected non-treated control. The nanoformula 5c-CNPs yielded the most outstanding results with the highest tachyzoite reduction percentage in both peritoneal fluid (98.1%) and liver impression smear (95.3%). Furthermore, the serum levels of liver enzymes (aspartate transaminase (AST) and alanine transaminase (ALT), and renal function tests (urea and creatinine) in mice were within normal limits which makes them more appealing candidates with proven safety. To the best of our knowledge, the present work is the first in silico and in vivo study proving the anti-Toxoplasma effect of isatin-1,2,3- triazoles which paves the way for further development of isatin and triazole-based leads for the treatment of toxoplasmosis.

Glycyrrhizin alleviated cisplatin-induced testicular injury by inhibiting the oxidative, apoptotic, hormonal, and histological alterations.

To evaluate the potential contribution of glycyrrhizin (GLZ) to mitigate the testicular toxicity linked to cisplatin (CIS) intoxication. 40 mature male Wistar albino rats (Rattus norvegicus albinus) were randomly divided into 4 equal groups (n = 10) for 60 days: the control group, CIS-treated group (single dose of 7 mg/kg, IP), GLZ-treated group (25 mg/kg, PO), and GLZ plus CIS-treated group. Blood and testis samples were examined using biochemical, histological, and immunohistochemical techniques. Semen samples were also obtained, and any abnormalities were reported. Serum follicle-stimulating hormone, luteinizing hormone, and testosterone levels were all markedly reduced by CIS. Oxidative stress and a significant reduction in levels of the antioxidant enzymes glutathione peroxidase, superoxide dismutase, and catalase were linked to CIS. Immunohistochemically, CIS showed diffuse, significantly positive immunolocalizations against the anti-caspase 3 antibody, indicating widespread apoptosis within the testicular parenchyma. Histopathologically, CIS showed diffuse coagulative necrosis of spermatogenic cells, necrotic Sertoli cells, intertubular edema, and Leydig cell hyperplasia. Moreover, CIS revealed a noteworthy increase in sperm abnormalities. Pre-coadministration and posttreatment with GLZ mitigated the majority of these detrimental consequences, and serum levels of antioxidant enzymes, luteinizing hormone, follicle-stimulating hormone, and testosterone were significantly elevated. Glycyrrhizin has been proven to be a strong antioxidant as well as antiapoptotic and cytoprotective against CIS testicular damage. The described model is a tool to evaluate the testicular protective impact of GLZ.

Humanin attenuates metabolic, toxic, and traumatic neuropathic pain in mice by protecting against oxidative stress and increasing inflammatory cytokine

Neuropathic pain is associated with diverse etiologies, including sciatica, diabetes, and the use of chemotherapeutic agents. Despite the varied origins, mitochondrial dysfunction, oxidative stress, and inflammatory cytokines are recognized as key contributing factors in both the initiation and maintenance of neuropathic pain. The effects of the mitochondrial-derived peptide humanin on neuropathic pain, however, remain unclear, despite its demonstrated influence on these mechanisms in numerous disease models. This study aimed to evaluate the effects of humanin on pain behavior in murine models of metabolic (streptozotocin/STZ), toxic (oxaliplatin/OXA), traumatic (sciatic nerve cuffing/cuff), and neuropathic pain. A secondary objective was to assess whether humanin modulates oxidative damage and inflammatory cytokine levels in these neuropathic pain models.Humanin (4 mg/kg) was administered intraperitoneally (i.p.) to BALB/c male mice with induced neuropathic pain over a period of 15 days, with pain thresholds assessed using hot plate, cold plate, and Von Frey tests. Serum levels of antioxidant enzymes, oxidative stress markers, and inflammatory/anti-inflammatory cytokines were measured via enzyme-linked immunosorbent assay (ELISA).In neuropathic pain-induced mice, humanin administration resulted in a statistically significant increase in pain threshold values in the STZ + Humanin, OXA + Humanin, and cuff + Humanin groups compared to their respective control groups (P < 0.05) over 15 days. Furthermore, humanin treatment significantly elevated antioxidant enzyme levels and anti-inflammatory cytokine concentrations, while reducing oxidative stress markers and pro-inflammatory cytokine levels compared to control groups (P < 0.01).These findings suggest that humanin exhibits therapeutic potential in the treatment of neuropathic pain induced by STZ, OXA, and cuff models. The ability of humanin to mitigate neuropathic pain through the suppression of oxidative stress and inflammatory cytokines indicates its promise as a novel therapeutic strategy.

Protective Effects of Lemna minor Linn. On Hepatic and Cognitive Impairments in Acetaminophen Induced Hepatic Encephalopathy in Rats

Aim: Lemna minor Linn., an aquatic plant, is a promising novel therapeutic agent that has been traditionally used in ethnobotanical practices as an ecofriendly supplement for the management of various ailments. This study involves the evaluation of ethanolic extract of Lemna minor Linn. against Paracetamol-induced Hepatic Encephalopathy using in vitro and in vivo Models. Methods: The acute oral toxicity study of the ethanolic extract of Lemna minor (EELM) was conducted following the OECD-425 guidelines over a 14-day period. A total of nine animals were used for this toxicity assessment. The EELM was tested in Paracetamol(PCM)-induced bioactivation animal model at two different dosages 200 and in comparison with silymarin as a standard compound. The In vivo experimental study was conducted using Sprague Dawley rats which was divided into 5 groups each group containing 6 animals so the total no of animals used in the study was 30 animals. The treatment groups included: normal control ( ), 100mg/kg silymarin (standard) and the EELM of two different doses of 200 and , p.o were administered to rats 10 hr before paracetamol ( ) treatment. Rats were orally administered their respective doses every day for total 30days. Paracetamol-induced oxidative liver damage disrupted normal levels of liver enzymes, total protein, and bilirubin, while also depleting antioxidant reserves. This oxidative stress was strongly associated with paracetamol toxicity, leading to a marked depletion of glutathione (GSH) and impairing both memory and cognitive function in the animals. Behavioral parameters are performed to evaluate the effect of drugs on cognitive behaviour of animals. Morris water maze test was performed to study how animals learn and remembers the spatial information relying on distal cues to locate the hidden platform in an opaque water. Additionally, elevated plus maze was performed to measures the anxious behaviour of rats, the criterion was tested based on the conflict between rats innate instincts to explore new environment and avoid open, well-lit areas. The potential protective effects of EELM was evaluated by measuring serum enzyme levels and antioxidants status in the liver and brain, further histopathological analysis was performed respectively. Results: The acute toxicity study did not report any mortality or toxicity signs in animals. PCM toxicity led to a statistically increase in the liver and body weight, along with brain water content. The PCM-intoxicated group exhibited a marked reduction in the level of superoxide dismutase (SOD) and glutathione (GSH) in the brain and liver, as well as an increase in lipid peroxidation and serum biomarkers (AST, ALT, ALP, and total bilirubin). EELM significantly ( ) reduced liver injury by inhibiting ALT, AST and ALP levels in serum. SOD, GSH and MDA liver content were significantly ( ) elevated by EELM, compared to PCM treated rats. Comparing the treatment and induced group, the treated group successfully recovered the activity of antioxidant levels and also been acknowledged for restored liver functioning by alleviating oxidative stress and also GSH level in brain was significantly increased by EELM and preserved the histology of brain, which was chronically produced over a period of 30 days. Conclusion: The findings of this investigation indicate the traditional use of Lemna minor in hepatoprotection and neuroprotection by regulating oxidative stress and mitigating reactive oxygen species (ROS). The insights gained from this research contribute to the development of novel therapeutic agents and paves the way for further studies on Lemna minor to enhance health outcomes, particularly in the management of neurodegenerative diseases.

L-carnitine ameliorates myocardial injury by alleviating endoplasmic reticulum stress via inhibition of PERK pathway in exertional heatstroke rats

Exertional heatstroke (EHS) is a life-threatening condition with potential for tissues and organs injury, including heart. Effective drug strategies to treat patients with EHS are warranted to unlock the therapeutic potential. Considering the cardioprotective effects of L-carnitine (LC), this study aimed to investigate the effects of LC on EHS-induced myocardial injury in rats and to explore the underlying mechanisms. Here, we found that LC exerted a greater protective effect on EHS-induced cardiac dysfunction and mortality, which also significantly attenuated certain negative effects, including increased myocardial apoptosis, pathological changes, and ultrastructural impairment, enhanced activity levels of such serum enzymes as AST, LDH, CK, and CK-MB, reduced BCL-2 expression, increased the expression of cleaved caspase-3 and the critical endoplasmic reticulum stress (ERS) indices like CHOP and GRP78 in EHS rats. Besides, pretreatment of EHS rats with PBA (4-Phenyl butyric acid), a chemical chaperone that attenuates ERS, restored BCL-2 expression, reduced the protein levels of cleaved caspase-3, CHOP, and GRP78. Furthermore, thapsigargin (TG), which induces ERS, enhanced the expression of BAX, cleaved caspase-3, CHOP, and GRP78, attenuated BCL-2 expression, and enhanced mitochondrial impairment in EHS + LC rats. Mechanismly, the protective effects of LC were mediated, at least partly, by inhibiting the activation of PERK pathway against ERS-associated myocardial damage. These results indicate that supplementation of LC might be a potential strategy to reduce myocardial injury by affecting ERS via inhibiting the PERK pathway against EHS.

Evaluation of the Safety and Efficacy of Curcumin-Synthesized Silver Nanoparticles in Rats Exposed to Chlorpyrifos During Puberty Development.

Silver nanoparticles (Ag-NPs) have garnered significant attention in recent years due to their therapeutic effects. Curcumin (CUR) has been utilized as a coating agent for synthesizing Ag-NPs, intended to act as a potential drug. This study was designed to evaluate the safety and efficacy of curcuminsynthesized silver nanoparticles on rats exposed to chlorpyrifos (CPF) during their pubertal development. Forty-two male Wistar rats, 23 days old, were selected and randomly divided into 7 groups (n=6) as follows: positive control, negative control, CPF (5 mg/kg), silver nanoparticles synthesized using curcumin at 40 μg/kg (CUR-Ag-NPs 40), CUR-Ag-NPs 80, CPF+ CUR-Ag-NPs 40, CPF+ CUR-AgNPs 80. All treatments were administered via gavage for 30 days. At the end of the study, rats were anesthetized using ketamine (50 mg/kg), and xylazine, (10 mg/kg) and blood was collected from the heart for serum analysis of liver enzymes, urea, and creatinine. Liver and kidney tissues were isolated for histopathological analysis. No significant differences were observed in serum levels of AST, ALT, and ALP enzymes as well as urea and creatinine levels among the different groups. Light microscopy observation revealed multifocal inflammatory mononuclear cell subsets in liver tissue associated with mild inflammatory mononuclear cell infiltration in the portal region in CPF, CUR-Ag-NPs 40, CUR-Ag-NPs 80, CPF+CUR-Ag-NPs 40, and CPF+CUR-Ag- NPs 80 groups. Histological examination of kidney tissue showed degenerative changes in the tubular epithelium, congestion, and mild infiltration of mononuclear inflammatory cells in the renal interstitial tissue in the CPF group, CUR-Ag-NPs 40, CUR-Ag-NPs 80, CPF+CUR-Ag-NPs 40 and CPF+CUR-Ag-NPs 80 groups. This study failed to establish the safety and efficacy of CUR-Ag-NP at 40 and 80 μg/kg in prepubertal rats exposed to CPF. However, further studies should be conducted to thoroughly characterize the efficacy of CUR-Ag-NP in developmental animal models.

A Relationship of Monoamine Oxidase-A with Serotonin in Violent Antisocial Behavior in Iraqi Prisoners

It is thought that the monoamine oxidase-A (MAOA) enzyme, which catalyzes key brain signaling chemicals like serotonin, noradrenaline, and dopamine, indirectly influences antisocial behavior by disrupting the neurotransmitter balance in brain regions and neural networks. This study aims to assess the MAOA enzyme level in serum and serotonin linked to antisocial behavior in cases in the prison of Baghdad City, Iraq. Blood samples were collected from (63) prisoners and (27) control groups, ages 18 years to 65 years, with a mean ± SD of 37.8 ± 8.8, all males, with different prison terms and different crimes for prisoners in the prison at Baghdad City, Iraq. MAOA and serotonin levels were measured in serum in prisoners and healthy men, and the results showed the serum levels of MAOA enzyme and serotonin were decreased in prisoners compared to the healthy (11.5 IU/ml vs. 19.5 IU/ml) and (79 IU/ml vs. 439 IU/ml), respectively, with the observed difference being significant (P &lt; 0.001(. The results of the relationship between education and social violence were: illiterate 11.1%, primary school 27%, secondary 52.4%, and university 9.5%. The median serum level of MAOA and serotonin in the age group 18–39 years was (11.3 IU/ml, 68.3 ng/ml), respectively, and in the age group 40–65 years was (13 IU/ml, 139 ng/ml), respectively.

A Case Report of Suspected Acute Pancreatitis with Elevated Serum Lipase

Objective: This study aimed to report the case of a patient with suspected acute pancreatitis who presented with elevated serum lipase levels and acute abdominal pain.Methods: A 26-year-old male presented with acute abdominal pain, vomiting, and elevated serum lipase levels. Anjung-san was administered along with acupuncture, moxibustion, and cupping therapy. The patient’s symptoms were evaluated daily using the numerical rating scale, abdominal palpation, and blood tests for pancreatic enzyme levels.Results: Following treatment, the patient’s symptoms, including abdominal pain, vomiting, and nausea, improved, and serum lipase levels returned to normal. No significant complications were observed during the hospital stay.Conclusion: Korean medicine treatment may effectively manage symptoms and reduce serum enzyme levels in patients with suspected acute pancreatitis.

Protective effect of magnetic water against AlCl3-induced hepatotoxicity in rats

This study aimed to examine whether or not aluminum chloride (AlCl3)-induced hepatotoxicity might be mitigated using magnetic water (MW) in rats. This study involved 28 adult male rats randomly assigned into the following 4 groups (7 rats/group): normal control (Cnt), MW, AlCl3, and Al Cl3 + MW. The Cnt group orally received normal saline, the MW group drank MW ad libitum for 2 months, and the AlCl3 and AlCl3 + MW groups were orally administered AlCl3 (40 mg/kg b.w.) alone or in combination with MW for 2 months, respectively. MW reduced AlCl3 toxicity as proved at functional, molecular, and structural levels. Functionally, MW reduced serum levels of liver enzymes (ALT, AST, ALP, GGT), while increased total proteins, and albumin. MW also restored redox balance in the liver (lower MDA levels, higher activities of CAT and SOD enzymes, and upregulated expression of NrF2, HO-1, and GST genes. Molecularly, MW downregulated hepatic expression of the epigenetic (HDAC3), inflammatory (IL1β, TNFα, NFκβ), and endoplasmic reticulum stress (XBP1, BIP, CHOP) genes. Structurally, MW enhanced liver histology. With these results, we could conclude that MW has the potential to ameliorate the hepatotoxic effects of AlCl3 through targeting oxidative stress, inflammation, epigenesis, and endoplasmic reticulum stress.

Histidine-trytophan-ketoglutarate cardioplegia reduces inflammatory response and serum levels of myocardial enzymes in newly developed right-thoracotomy rat model

The objective of this research was to establish a rat model for cardiopulmonary bypass (CPB) with cardiac arrest and resuscitation that is both practical and economical and simulates clinical cardiac surgery. Concurrently, the study aimed to evaluate the myocardial protective effects conferred by histidine–tryptophan–ketoglutarate (HTK) cardioplegia. Thirty rats were randomly assigned to three groups: the histidine–tryptophan–ketoglutarate (HTK), 4:1 blood cardioplegia (BC) and del Nido cardioplegia (DN) groups. The cardiopulmonary bypass (CPB) procedure was implemented and sustained for a duration of one hour. Subsequent to the cessation of CPB, the rats were subjected to monitoring and observation for an additional two hours. Following this observation period, the heart and blood samples were procured for subsequent analysis. During CPB, the average hematocrit level was significantly below the typical physiological range (P < 0.001). Histopathological scores were notably lower in the HTK group in contrast to the BC group (P < 0.001) or the DN group (P < 0.001). At 2 h after weaning off CPB, the levels of CK and CKMB in the DN and BC groups were notably elevated compared to the HTK group (P < 0.001). The levels of IL-6 and TNF-α proteins were notably increased in all three groups (P < 0.001), with the BC and DN groups showing higher increases compared to the HTK group (P < 0.001). This compact animal model of cardiopulmonary bypass (CPB) with cardiac arrest and resuscitation might allow for both the study of myocardial ischemia-reperfusion injury as well as cardioprotective strategies. HTK cardioplegia could reduce inflammatory response and serum levels of myocardial enzymes in this newly developed right thoracotomy rat model.

A Scoping Review on Hepatoprotective Mechanism of Herbal Preparations through Gut Microbiota Modulation.

Liver diseases cause millions of deaths globally. Current treatments are often limited in effectiveness and availability, driving the search for alternatives. Herbal preparations offer potential hepatoprotective properties. Disrupted gut microbiota is linked to liver disorders. This scoping review aims to explore the effects of herbal preparations on hepatoprotective mechanisms, particularly in the context of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and hepatic steatosis, with a focus on gut microbiota modulation. A systematic search was performed using predetermined keywords in four electronic databases (PubMed, Scopus, EMBASE, and Web of Science). A total of 55 studies were included for descriptive analysis, covering study characteristics such as disease model, dietary model, animal model, intervention details, comparators, and study outcomes. The findings of this review suggest that the hepatoprotective effects of herbal preparations are closely related to their interactions with the gut microbiota. The hepatoprotective mechanisms of herbal preparations are shown through their effects on the gut microbiota composition, intestinal barrier, and microbial metabolites, which resulted in decreased serum levels of liver enzymes and lipids, improved liver pathology, inhibition of hepatic fatty acid accumulation, suppression of inflammation and oxidative stress, reduced insulin resistance, and altered bile acid metabolism.

N-Acetyltransferase 2 gene polymorphism and its serum levels in vitiligo patients

ABSTRACT Background Although numerous mechanisms are involved in vitiligo pathogenesis, few studies correlate N-acetyltransferase 2 to this disease. Aim To assess the N-acetyltransferase 2 (rs1799929) gene and its serum levels in vitiligo patients. Subjects and methods In this case-control study, 65 vitiligo cases were compared to 65 age- and sex-matched healthy controls. Serum NAT2 levels and the NAT2 gene polymorphism (rs1799929) were evaluated using ELISA and real-time PCR, respectively. Results Serum N-acetyltransferase 2 levels were significantly lower in cases than in controls, 1.24 ± 0.31 vs. 2.01 ± 0.46 (p = 0.001). CC genotype was more dominant in controls (58.5%) than in cases (20%). TT and CT genotypes were more dominant in cases (30.8% and 49.2%) than in controls (13.8% and 27.7%), respectively (p = 0.001). The C allele was more prominent in controls (72.3%) than in cases (44.6%) while the T allele was more dominant in cases (55.4%) than in controls (27.7%) (p = 0.001). N-acetyltransferase 2 slow acetylator phenotype (TT genotype) was higher in cases (30.8%) than in controls (13.8%) and rapid acetylator phenotypes (CC and CT genotypes) were higher in controls (86.2%) than in cases (69.2%) (p = 0.035). Conclusion Slow acetylator genotype (TT) of NAT2 gene (rs1799929) and low serum levels of NAT2 enzyme might play a role in the susceptibility and pathogenesis of vitiligo.