BACKGROUND:polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder often associated with insulin resistance and metabolic-associated fatty liver disease (MAFLD), both linked to impaired autophagy. This study evaluates the effects of metformin and levothyroxine on autophagy regulation in a PCOS-induced MAFLD rat model. MATERIALS AND METHODS:PCOS was induced in female Wistar rats by testosterone enanthate (7.5 mg, E16-19). Post-weaning, rats were assigned to control, model, metformin (300 mg kg-1 per day), levothyroxine (50 μg kg-1 per day), or combination groups. Body/liver weight, serum markers (ALT, AST, TSH, lipid profile, testosterone, LH, estradiol), insulin sensitivity, autophagy-related proteins (LC3II, ATG7, p62, CK18), and histology were assessed. Network pharmacology, protein-protein interaction, KEGG enrichment, and molecular docking were performed. RESULTS:combination therapy reduced body weight (10.29%) and liver weight (37.08%) and lowered ALT (26.17%), AST (42.69%), TSH (77.9%), cholesterol (41.32%), triglycerides (32.37%), and LDL (43.42%). Testosterone and LH declined (37.25%, 14.43%), while estradiol rose (37.4%). HOMA-IR decreased by 51.85%. Autophagy markers (CK18, LC3II, P62, ATG7) were suppressed, with improved hepatic and ovarian histology. Network analysis identified NOS2, KRT18, MAP1LC3B, ATG7, and SQSTM1 as key targets, with KEGG pathways implicated in autophagy, mitophagy, ferroptosis, and apelin signaling. Docking analysis showed stronger binding of levothyroxine to LC3II and ATG7, suggesting a direct modulatory role. CONCLUSION:metformin and levothyroxine synergistically improve PCOS-related MAFLD by restoring autophagy and metabolic-endocrine balance. System-level and docking analyses support autophagy regulation as a key therapeutic mechanism, highlighting the potential role of levothyroxine in modulating autophagy.

Chronic relapsing colonic inflammation, specifically ulcerative colitis (UC), causes persistent mucosal injury and disrupts the gut-brain axis. This disruption leads to basal ganglia neuroinflammation and ultimately extrapyramidal motor dysfunction. Dysregulation of the Dectin 1/leucine-rich repeat kinase 2 (LRRK2)/α-synuclein (αSyn) signaling exacerbates inflammation. This study investigated whether modulation of this pathway affects UC progression and is associated with motor deficits using trimetazidine (TMZ) treatment in a Bagg albino c (BALB/c) mice model. Furthermore, we examined the role of this pathway through molecular docking followed by molecular dynamics simulations to evaluate the plausibility of TMZ interactions with Dectin-1, LRRK2, and α-syn proteins. Our results indicate that TMZ improved behavioral changes and also significantly reduced serum interferone-γ (IFN-γ) and NF-kB levels, along with decreased Dectin-1, LRRK2, and αSyn expression. TMZ also mitigated colonic inflammation, as shown by reducing fecal calprotectin and fecal occult blood, supported by histological examinations. Furthermore, TMZ restored autophagic flux by reducing P62 accumulation and enhancing LAMP2 expression. Molecular docking and dynamics confirmed TMZ binding to Dectin-1, LRRK2, and αSyn, through hydrophobic and hydrophilic interactions. These findings suggest a potential molecular basis for the observed associations between the Dectin-1/LRRK2/α-synuclein axis and UC-related motor dysfunction, warranting further experimental validation, establishing TMZ's therapeutic potential for managing colonic inflammation and associated neurological manifestations.

Rheumatoid Arthritis is a complex chronic auto-immune systemic illness. It is primarily characterized by synovial hyperplasia and localized pro-inflammatory cytokine production that causes chronic synovitis and a long-lasting inflammation of the joints and bones. The study's goal was to look into the potential anti-arthritic effects of trimetazidine in a rat model of Freund’s complete adjuvant (FCA)-induced arthritis, which has many clinical and biochemical similarities to rheumatoid arthritis (RA). The underlying antirheumatoid arthritis mechanism, as well as its impact on TLR4/NFKB pathway were investigated to understand and confirm its potential efficacy in RA treatment. Our study was based on 4 groups, control group received saline injections, trimetazidine (7.2 mg/kg/day) treated group, methotrexate (0.75 mg/kg/week) treated group and combination group that received both medications in the same doses for 21 days. The degree of ipsilateral paw swelling, ankle diameter, body weight, tissue expression levels of TLR4(toll like receptor) and NFKB (nuclear factor kappa b) in paw, and serum ACPA (anticitrullinated protein antibodies) were all measured. With a slight but not statistically significant impact on ankle diameter, trimetazidine and methotrexate considerably reduced the arthritic symptoms as indicated by ipsilateral paw volume. It had no discernible impact on body weight. Together with the overall improved synovial hyperplasia and cartilage disarrangements, TLR4 and NFKB expression in synovial tissue were reduced. In a rat model of CFA-induced arthritis, trimetazidine displays a considerable anti- inflammatory impact that is even better than methotrexate and has the potential to be anti-arthritic. Additionally, there is a large additive effect between the two medications.

Abstract Background Acute liver failure (ALF) is one of the emergency conditions. Carbon tetrachloride (CCl4) has been widely used to induce experimental hepatic damage. Bone marrow mesenchymal stem cell derived (BM-MSC) exosomes are broadly applied to regenerative approaches for various disorders serving the therapeutic effects of MSCs. Aim of the Work The study analyzed microscopically and biochemically, the regenerative power of the BM-MSC exosomes on the experimentally induced acute hepatic injury. Materials and Methods Fifty-five male adult Wistar albino rats were randomly divided into three groups: Group (I) control group, group II [given a single intraperitoneal injection of carbon tetrachloride (CCl4) (3% vol/vol in olive oil) at 0.05 ml/kg body weight] and group III [given a single tail vein injection of 50 μg of BM-MSC exosomes in 100 μl phosphate buffered saline 24 hours post-CCl4]. The rats were sacrificed after seven days. Biochemical analysis of AST and ALT was performed. Histological examination of liver tissue was performed through light microscopy of hematoxylin and eosin and Masson trichrome stained sections. Transmission electron microscopy (TEM) of liver tissue was carried out. Morphometric and statistical studies were done. Results By light microscopy, H&E-stained sections of Group II (CCl4 treated) revealed altered hepatic architecture with focal cellular infiltration. Congestion and dilatation of portal veins with periportal cellular infiltration were detected. Widening and endothelial discontinuity of the central veins and disorganization and obliteration of some blood sinusoids were demonstrated. Most hepatocytes appeared with darkly acidophilic cytoplasm and condensed nuclei, while others appeared with pyknotic nuclei with vacuolated cytoplasm. In Masson trichrome stained sections, there was a significant increase in the collagen fibers around the central veins and portal triads, and between hepatic cords. TEM examination, hepatocytes displayed irregular heterochromatic nuclei and rarified cytoplasm with plenty of lipid droplets. Hepatic stellate cells were devoid of lipid droplets. The epithelial cell lining the bile ductules had few short microvilli Inflammatory cells were seen near the ductular basal border. Biochemically, there was a significant increase in both ALT & AST levels in group II. The exosomes treated group (III) revealed marked amelioration of the previously mentioned histopathological and biochemical changes compared to the control group. Conclusion The acute CCl4 induced injury was significantly attenuated by BM-MSC exosomes therapy, and is characterized by an increase in hepatocyte proliferation, significant regression of collagen deposition in the liver tissue and marked attenuation of hepatocellular damage, both structurally and biochemically.

Rheumatoid arthritis (RA) is a debilitating autoimmune condition characterized by chronic synovitis, joint damage, and inflammation, leading to impaired joint functionality. Existing RA treatments, although effective to some extent, are not without side effects, prompting a search for more potent therapies. Recent research has revealed the critical role of FAS-associated death domain protein (FADD) microvesicular shedding in RA pathogenesis, expanding its scope beyond apoptosis to include inflammatory and immune pathways. This study aimed to investigate the intricate relationship between mi-RNA 128a, autoimmune and inflammatory pathways, and adenosine levels in modulating FADD expression and microvesicular shedding in a Freund’s complete adjuvant (FCA) induced RA rat model and further explore the antirheumatoid potency of trimetazidine (TMZ). The FCA treated model exhibited significantly elevated levels of serum fibrogenic, inflammatory, immunological and rheumatological diagnostic markers, confirming successful RA induction. Our results revealed that the FCA-induced RA model showed a significant reduction in the expression of FADD in paw tissue and increased microvesicular FADD shedding in synovial fluid, which was attributed to the significant increase in the expression of the epigenetic miRNA 128a gene in addition to the downregulation of adenosine levels. These findings were further supported by the significant activation of the TLR4/MYD88 pathway and its downstream inflammatory IkB/NFB markers. Interestingly, TMZ administration significantly improved, with a potency similar to methotrexate (MTX), the deterioration effect of FCA treatment, as evidenced by a significant attenuation of fibrogenic, inflammatory, immunological, and rheumatological markers. Our investigations indicated that TMZ uniquely acted by targeting epigenetic miRNA128a expression and elevating adenosine levels in paw tissue, leading to increased expression of FADD of paw tissue and mitigated FADD microvesicular shedding in synovial fluid. Furthermore, the group treated with TMZ showed significant downregulation of TLR4/MYD88 and their downstream TRAF6, IRAK and NF-kB. Together, our study unveils the significant potential of TMZ as an antirheumatoid candidate, offering anti-inflammatory effects through various mechanisms, including modulation of the FADD-epigenetic regulator mi-RNA 128a, adenosine levels, and the TLR4 signaling pathway in joint tissue, but also attenuation of FADD microvesicular shedding in synovial fluid. These findings further highlight the synergistic administration of TMZ and MTX as a potential approach to reduce adverse effects of MTX while improving therapeutic efficacy.

Acute heart failure (AHF) is one of the most common diseases in old age that can lead to mortality. Systemic hypoperfusion is associated with hepatic ischemia–reperfusion injury, which may be irreversible. Ischemic hepatitis due to AHF has been linked to the pathogenesis of liver damage. In the present study, we extensively investigated the role of mitochondrial dynamics-related proteins and their epigenetic regulation in ischemic liver injury following AHF and explored the possible hepatoprotective role of carvedilol. The biochemical analysis revealed that the ischemic liver injury following AHF significantly elevated the activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes, the level of total and direct bilirubin, and the expression of hepatic mitogen-activated protein kinase (MAPK), dynamin-1-like protein (DNM1L), and hepatic miRNA-17. At the same time, it significantly reduced the serum albumin level, the activity of hepatic superoxide dismutase (SOD), and the expression of mitochondrial peroxisome proliferator-activated receptor-1α (PGC-1α), and mitofusin 2 (Mtf2). The histological examination of the liver tissue revealed degenerated hepatocytes. Interestingly, administration of carvedilol either prior to or after isoprenaline-induced AHF significantly improved the liver function and reversed the deterioration effect of AHF-induced ischemic hepatitis, as demonstrated by biochemical, immunohistochemical, and histological analysis. Our results indicated that the hepatoprotective effect of carvedilol in ameliorating hepatic ischemic damage could be attributed to its ability to target the mitochondrial dynamics-related proteins (Mtf2, DNM1L and PGC-1α), but also their epigenetic regulator miRNA-17. To further explore the mode of action of carvedilol, we have investigated, in silico, the ability of carvedilol to target dynamin-1-like protein and mitochondrial dynamics protein (MID51). Our results revealed that carvedilol has a high binding affinity (−14.83 kcal/mol) toward the binding pocket of DNM1L protein. In conclusion, our study highlights the hepatoprotective pharmacological application of carvedilol to attenuate ischemic hepatitis associated with AHF.

Testicular torsion (TT) is the most common urological emergency in children and young adults that can lead to infertility in many cases. The ischemia-reperfusion (IR) injury due to TT has been implicated in the pathogenesis of testicular damage. The main pathological mechanisms of contralateral injury after ipsilateral TT are not fully understood. In the presented study, we investigated the molecular and microscopic basis of ipsilateral and contralateral testicular injury following ipsilateral testicular torsion detorsion (T/D) and explored the possible protective role of vitamin D3. The biochemical analysis indicated that IR injury following T/D significantly decreased the activity of testicular glutathione peroxidase (GPx) enzyme, level of serum testosterone, serum inhibin B, and expression of testicular miRNA145, while increased the activity of testicular myeloperoxidase (MPO) enzyme, level of testicular malondialdehyde (MDA), level of serum antisperm-antibody (AsAb), and expression of ADAM-17. The histological and semen analysis revealed that torsion of the testis caused damages on different tissues in testis. Interestingly, administration of vitamin D3 prior to the IR injury reversed the deterioration effect of IR injury on the testicular tissues as indicated by biochemical and histological analysis which revealed normal appearance of the seminiferous tubules with an apparent decrease in collagen fiber deposition in both ipsilateral and contralateral testes. Our results revealed that the protective effect of vitamin D3 treatment could be attributed to target miRNA145 and ADAM17 protein. To further investigate these findings, we performed a detailed molecular modelling study in order to explore the binding affinity of vitamin D3 toward ADAM17 protein. Our results revealed that vitamin D3 has the ability to bind to the active site of ADAM17 protein via a set of hydrophobic and hydrophilic interactions with high docking score. In conclusion, this study highlights the protective pharmacological application of vitamin D3 to ameliorate the damages of testicular T/D on the testicular tissues via targeting miRNA145 and ADAM17 protein.

Potentiometric sensors have a great influence on the determination of most various compounds in their matrices. Therefore, efficient and new sensors were introduced to measure sodium Deoxycholate (NaDC) as a bile acid salt. These sensors are based on NaDC imprinted polymer (MIP) as sensory element. The MIP beads were synthesized using thermal polymerization pathway, in which acrylamide (AAm), ethylene glycol dimethacrylate (EGDMA), NaDC, and benzoyl peroxide (BPO) were used as the functional monomer, cross-linker, template, and initiator, respectively. The proposed sensors were fabricated using a coated screen-printed platform and the sensing membrane was modified by single-walled carbon nanotubes (SWCNTs) as an ion-to-electron transducer. The sensors exhibited high sensitivity that reached 4.7 × 10−5 M of near-Nernestian slope (−60.1 ± 0.9 mV/decade, r2 = 0.999 (n= 5)). In addition, the sensors revealed high selectivity, long lifetime, high potential stability, and conductivity that ensure reproducible and accurate results over a long time. MIP characterization was performed using Fourier Transform-Infrared (FT-IR) and a scanning electron microscope (SEM). Regarding the interaction of NaDC with serum albumin (SA), albumin is determined in human serum samples as human serum albumin (HSA), which was collected from different volunteers of different ages and gender.

Background: Thioacetamide (TAA), a known industrial toxic agent, is extensively used in animal studies for induction of hepatic necrosis, fibrosis and cirrhosis, also reported to be nephrotoxic through induction of oxidative stress.Propolis, bee glue, is known by its antioxidant and anti-inflammatory properties. Aim of Study:This work aimed to evaluate the potential protective effect of propolis on TAA-induced hepatorenal damage and to evaluate the efficacy of Kidney Injury Molecuole-1 (KIM-1) in early detection of renal injury. Material and Methods:This study was performed on 24 adult male albino rats, divided into 3 groups; (I) Control group, (II) TAA-group (TAA was given in a dose of 50mg/kg /day intraperitoneally, 5 days/week for 2 weeks), (III) TAApropolis treated group (TAA was given in the same way as in TAA-group, propolis was given in a dose of 500mg/kg/day by gavage, 5 days/week for 2 weeks).All studied rats were subjected to determination of initial and final body weight, body weight percent change, absolute and relative liver and kidney weight, as well as assessment of hepatic function by serum Alanine Transaminase (ALT) and Aspartate Transaminase (AST), renal function by serum urea, creatinine and potassium (K+) level, with determination of renal tissue oxidative stress markers; Malondialdehyde (MDA) and Glutathione-S-Transferase (GST), inflammatory marker; Myeloperoxidase (MPO), renal tissue damage marker; Kidney Injury Molecule-1 (KIM-1).In addition, specimens of liver and kidney were taken and processed for light microscopic studies.Results: TAA induced hepatotoxic and nephrotoxic effect that was evident by the significantly increased serum ALT, AST, urea and creatinine, with significant decrease in serum K + level as well as significantly increased renal tissue MDA, GST, MPO and KIM-1 when compared with control group.Treatment with propolis caused significant reduction in serum ALT, AST, urea and creatinine, with significant elevation in serum K + as well as significant reduction in renal tissue MDA, GST, MPO and KIM-1 when compared to the TAA group, but still significantly higher compared to controls except for

A novel single-piece all-solid-state ion-selective electrode (SC/ISE) based on carbon-screen printed is introduced. Polyaniline (PANI) is dissolved in a membrane cocktail that contains the same components used for making a conventional ion-selective polyvinyl chloride (PVC) matrix membrane. The membrane, having the PANI, is directly drop-casted on a carbon substrate (screen-printed-carbon electrode). PANI was added to act as an intermediary between the substrate and the membrane for the charge transfer process. Under non-equilibrium sensing mechanism, the sensors revealed high sensitivity towards 2,4-dichlorophenol (DCP) over the linearity range 0.47 to 13 µM and a detection limit 0.13 µm. The selectivity was measured by the modified separate solution method (MSSM) and showed good selectivity towards 2,4-DCP over the most commonly studied ions. All measurements were done in 30 mm Tris buffer solution at a pH 5.0. Using constant-current chronopotentiometry, the potential drift for the proposed electrodes was checked. Improvement in the potential stability of the SPE was observed after the addition of PANI in the sensing membrane as compared to the corresponding coated-wire electrode (membrane without PANI). The applicability of the sensor has been checked by measuring 2,4-DCP in different water samples and the results were compared with the standard HPLC method.

Introduction: Moringa oleifera is a tropical tree whose leaves are rich in antioxidant compounds. Paracetamol hepatotoxicity is a significant public health concern. Aim: The aim of this study was to investigate the possible protective role of Moringa oleifera leaves (MOL) aqueous extract on paracetamol induced liver injury in adult male albino rats.Materials and Methods: Forty adult male albino rats were used in the current study and were divided into four equal groups,: Group I served as control; Group II were given MOL for 14 days; Group III were given water for 7 days followed by paracetamol for another seven days; Group IV were given MOL for 14 days and Paracetamol on the seventh day for 7days.All medications were given by nasogastric tube. Specimens of liver were excised and processed for histological and histochemical studies. Blood samples were collected for biochemical study. Statistical analysis of the results was done.Results: MOL administration in group II didn't affect hepatic architecture or liver function tests. There was a significant increase in glutathione peroxidase and catalase activity and no significant difference in malondialdehyde level as compared to control. Paracetamol administration led to vacuolization of hepatocytes, cellular infiltrations and congestion in central and portal veins, with apparent increase in number of cholangiocytes. There were also significant decrease in the area percentage of PAS positive granules and significant decrease in area percentage of collagen fibers as compared to control. By electron microscope, distorted mitochondria, decrease of rough endoplasmic reticulum and increase of smooth endoplasmic reticulum & collagen fibrils were observed. Administration of Moringa before paracetamol ameliorated damaging effects of paracetamol. Minimal cellular infiltrations and apparent increase in number of cholangiocytes were still observed. Conclusion: MOL extracts could protect the liver against paracetamol effects through inhibition of lipid peroxidation and enhancement of antioxidant enzymes.

The role of hepatic free cholesterol (FC) in nonalcoholic steatohepatitis (NASH) is raised up and the intervention with cholesterol synthesis will be a potential therapeutic target. This study investigated the hepatoprotective effect of mevalonic acid pathway inhibition by Zoledronic acid (ZA) on the hepatic changes associated with high fat diet (HFD) in rats.Thirty two male Wistar rats were used. They were divided into 2 groups: (I) control naïve (II) NASH: induced by HFD for 12 weeks, this group is subdivided into (A) NASH untreated (B)NASH + ZA (50ug/kg/week) i.p. for 12 weeks (C) NASH + ZA (100μg/kg/week) i.p. for 12 weeks. Portal pressure (PP), liver enzymes AST and ALT, serum glucose, lipid profile, hepatic levels of tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), FC and triglyceride (TG), histopathological changes and expression of both hepatic alpha smooth muscle actin (α-SMA) and Caspase-3 were measured. ZA significantly prevented portal hypertension, worsening in liver function, and dyslipidemia. The hepatic levels of TNF-α, VEGF, FC and TG were significantly decreased in comparison to NASH untreated group. ZA hindered the histopathological changes induced by HFD. ZA inhibited the expression of hepatic α-SMA and Caspase-3 with significant difference favor the high dose intervention. ZA in a dose related manner prevents the hepatic pathological effects of chronic HFD ingestion in rats. This may be largely mediated by its ability to reduce TNF-α and hepatic FC.

Long acting non-coding RNAs lncRNAs HOX Transcript Antisense RNA (HOTAIR) is cardioprotective and mediates its effect through sirtulin 1 (SIRT1). The decrease in HOTAIR expression predisposes to various types of cardiomyopathy. We aimed to investigate whether decrease HOTAIR expression is involved in cirrhotic cardiomyopathy or not and the role of glucagon like peptide 1 receptor (GLP-1 receptor) in facilitating its effect through studying the effect of a exenatide (EXA), on cardiac function as well as the expression of some relevant bio-molecules. Rats were used and divided into: naïve, EXA, Thioacetamide (TAA) and TAA + EXA groups. ECG, dobutamine stress test (DST) were done. AST, ALT, fasting blood glucose, troponin I were measured. Cardiac HOTAIR & SIRT1, hepatic and cardiac GLP-1 receptor expression levels were investigated in addition to histological studies. Our results showed that EXA administration in control rats produced no significant changes. TAA induced cirrhosis with insulin resistance and significant changes in cardiac functions. GLP-1 receptor, HOTAIR and SIRT1 expression in cardiac tissue were significantly decreased with a significant increase in troponin I. EXA + TAA group showed a restoration of the hepatic architecture and function. EXA treatment produced significant improvement in cardiac parameters and was associated with increasing the expression of cardiac GLP-1 receptor, HOTAIR. The cardiac muscle showed an apparent decrease in collagen fibers. So we can conclude that EXA promotes the protective effect of HOTAIR on cardiac structure and function in rat model of cirrhosis which may introduce a new therapeutic strategy in cirrhotic cardiomyopathy.

Introduction: Every new technological product brings certain disadvantages threatening human health.Electromagnetic fields (EMF) emitted from cell phones may exert a detrimental influence on human health and may affect man`s cognitive and reproductive systems.Mobile phones are carried mainly near the head during talking and they are also kept in trousers pockets in close distance to testis.Aim: To study the effect of single or multiple exposure to different doses of EMF from mobile phone on the structure of hippocampus and testis in adult albino Wistar rats Materials and Methods: Thirty adult male albino Wistar rats were divided into three equal groups.Group I (control), group II (single mobile exposure giving 900Hz) and group III (multiple mobile exposure giving 2700HZ).Rats were exposed to EMW for 120 minutes/day, 6 days per week for ten weeks.Animals were sacrificed 24 hours after the last exposure.Hippocampus and testis were harvested form all rats.They were subjected to proper histological techniques.Semen analysis, morphometric and statistical studies were also done.Results: In single exposure group, degeneration of some pyramidal and granule cells of the hippocampus were noticed.Vacuolations were also seen between spermatogenic cells with some abnormalities of sperm structure.While in multiple exposure group, apparent increase number of degenerated neurons and significant decrease in thickness of pyramidal and granule layers of hippocampus were noticed.Testis showed intercellular vacuolations, significant decrease in thickness of germinal epithelium and seminiferous tubules and a significant increase in mean area percentage of collagen fibers and caspase-3 reaction.Many sperm abnormalities were also detected in semen analysis.Conclusions: Exposure to EMF causes significant changes in the structure of hippocampus and testis in a dose dependent manner.

Introduction Cholestasis has been implicated in the development of hepatocellular injury. Some suggested statins (cholesterol-lowering agents) as potential candidates for the treatment of cholestasis. Other studies have shown that statins may exert a negative effect on the liver parenchyma. Aim The aim of this study was to investigate the role of rosuvastatin, as one of the statins, in hepatic cholestasis induced by common bile duct ligation (BDL) in rats. Materials and methods Twenty-eight male albino rats were used in this study and were divided into four groups: group I served as control; group II was the sham group; group III rats underwent BDL operation; and group IV rats received 0.45 mg/kg/day of rosuvastatin orally after BDL for 2 weeks. Specimens of the liver were excised and processed for histological and immunohistochemical studies. Blood samples were collected for biochemical study. Statistical analysis of some results was performed. Results Cholestasis induced histological changes in the liver, including proliferation of bile ducts and mononuclear cellular infiltration at the portal tracts. Some hepatocytes appeared swollen with vacuolated cytoplasm, whereas others showed disintegrated nuclei (karyorrhexis). This was confirmed by a significant increase in the mean area% of immunostaining for caspase-3. Moreover, the collagen fiber content was apparently increased. At the same time the mean area% of immunostaining for α smooth muscle actin was significantly increased. Intake of rosuvastatin partially reversed some of these changes. Conclusion Rosuvastatin partially reversed hepatic injury caused by cholestasis following BDL.

Introduction The success of endodontic surgery depends on the histocompatibility of the root-end filling material. Applications of nanotechnology improve their performance. Aim of the work Aim of the work was to compare the effect of a mineral trioxide aggregate (MTA)and a bioceramic nanoparticulate bioaggregate (BNB) on the histological structure of draining axillary lymph nodes of adult male albino rats after their surgical implantation into the skin. Materials and methods Forty adult male albino rats were divided into control and experimental groups.The latter was subdivided into MTA and BNB surgically implanted subgroups. After 7 days, the rats were sacrificed. Paraffin sections from both the proximal part of the dorsal skin and draining axillary lymph nodes were processed for H&E staining.Lymph node sections were further subjected to silver reticulin, Verhoeff’s Van Gieson stains as well as kappa light chains. Quantitative assessments and statistical analysis of the results were carried out. Results There was an increase in mononuclear inflammatory cells infiltrating the skin in the MTA subgroup. Lymph nodes of the MTA subgroup showed a marked decrease in the lymphocyte content of lymphatic nodules, wide lymph sinuses, multinucleate giant cells, and many macrophages. In the BNB-treated subgroup, lymphatic nodules had wide corona and small germinal centers. Reticular and collagen fibers were increased in the MTA subgroup. Kappa light chains’ immunoreactions were strong positive in MTA and mild positive in BNB subgroups. A highly significant increase in the mean area% of all fibers and kappa light chain immunoexpression of lymph nodes of the MTA subgroup were observed. Conclusion and recommendation MTA had less biocompatibility. BNB showed limited signs of acute inflammation. BNB is an up-to-date alternative to the currently used root-end filling materials. The chronic effects caused by BNB may require further study.