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Acetaminophen (APAP), widely used as an analgesic-antipyretic drug, can cause liver and kidney damage at high doses. This study explored the protective effects of a mucolytic agent and an antioxidant Ambroxol (AMB), against APAP-induced toxicity in rats. The experiment included four groups of Wistar albino rats each having 6 animals in both sexes: a control group, an AMB-only group (50 mg/kg orally), an APAP-only group (1000 mg/kg intraperitoneally), and a combination APAP+AMB group. Twenty-four hours following the administration of APAP administration, rats were sacrificed. Measurements of blood levels of liver enzymes (AST, ALT, ALP, LDH), kidney function markers (Urea, Creatinine), and antioxidant enzymes (SOD, GPx) were performed. GPx and SOD activities were also assessed in hepatic and renal tissue samples. Histological examination of hepatic and renal tissues was conducted using Haematoxylin and Eosin staining. Results showed that APAP significantly increased liver enzymes, BUN, and Creatinine levels, indicating hepatorenal damage. This was accompanied by a decrease in plasma GPx and SOD activities. However, AMB treatment significantly mitigated these changes. It improved enzyme activities and increased hepatic GPx. Histologically, the APAP group showed liver cell damage, necrosis, haemorrhage, and inflammation, which were notably reduced in the AMB-treated group. This study suggests that Ambroxol effectively counters APAP-induced hepatorenal damage by restoring antioxidant enzyme levels and normalizing functional enzyme activities, highlighting its potential as a protective agent. [ABSTRACT FROM AUTHOR]

Ischemia-reperfusion injury is a clinical condition that poses life-threatening risks and can be caused by diseases or operations such as trauma, shock, and gastric dilatation volvulus. The objective of this study was to examine the effect of oxytocin on intestinal damage in rats induced by experimental ischemia-reperfusion injury. Three groups of Wistar albino rats were established: a control group (CTR, n=6), an intestinal ischemia-reperfusion group (I-IR, n=6), and an intestinal ischemia-reperfusion with oxytocin group (I-IR+Oxt, n=6). The I-IR+Oxt group received an intraperitoneal injection of 1 mg/kg oxytocin 30 minutes before anesthesia. In the I-IR and I-IR+Oxt groups, the superior mesenteric artery was ligated for 1 hour to induce ischemia-reperfusion injury, followed by one hour of reperfusion by opening the ligatures. At the end of the reperfusion period, the rats were euthanized, and blood and intestinal tissue samples were collected. From the blood samples, ALT, ALP, AST, LDH, BUN, creatinine, IL-1β, and TNF-α concentrations were evaluated. Tissue samples were analyzed for IL-1β, TNF-α, and MDA activity. Serum and tissue IL-1β and TNF-α concentrations were higher in both the I-IR and I-IR+Oxt groups compared to the CTR group. However, these levels were found to be lower in the I-IR+Oxt group compared to the I-IR group. The histopathological analysis showed that the I-IR+Oxt group had better epithelial regeneration and less inflammatory cell infiltration compared to the I-I/R group. In conclusion, oxytocin inhibited the release of IL-1β and TNF-α and the harmful effect of I/R on intestinal cells. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to investigate the potential protective effects of N‐acetyl‐L‐cysteine (NAC) against apical periodontitis (AP) in rats with adriamycin (ADR)‐induced kidney and heart diseases. Methodology: Fourty‐eight Wistar albino rats were divided into six groups: (1) Control group, (2) ADR group (1 mg/kg/day ip for 10 days), (3) AP Group (1st mandibular molar tooth), (4) AP + ADR Group, (5) AP + NAC group (150 mg/kg/day ip), and (6) AP + ADR + NAC group. After 3 weeks, the rats were decapitated and blood and tissue samples (heart, kidney, and jaw) were collected. Tissue samples were evaluated by biochemical (inflammatory cytokines and hemodynamic parameters) and radiological analyses. One‐way anova with Tukey post hoc tests was used to compare data, considering p <.05 as statistically significant. Results: The serum levels of TNF‐α, IL‐1β, BUN, Creatinine, CK, and LDH were elevated in the test groups compared with the control group, and treatment with NAC reduced these levels (p <.05). Heart and kidney tissue analysis showed a higher heart‐to‐body weight ratio (HW/BW) and kidney‐to‐body weight ratio (KW/BW) in the test groups compared with the control group (p <.05). No significant differences in HW/BW and KW/BW were found between the control and AP + NAC groups. Volumetric apical bone resorption analysis showed an increase in periapical radiolucencies in AP‐induced groups indicating apical periodontitis. NAC treatment reduced the total area and volume of resorption cavities (p <.05). Conclusions: The results suggest that NAC's antioxidant and anti‐inflammatory effects can reduce adriamycin‐mediated heart and kidney damage and may have a positive effect on apical periodontitis in individuals with nephropathy and cardiomyopathy. [ABSTRACT FROM AUTHOR]

Objective: 5-Fluorouracil (5-FU), a widely administered anti-cancer drug, causes gastrointestinal damage through various mechanisms. This study aimed to investigate the ameliorative effect of silk fibroin (SF), which has anti-inflammatory and antioxidant properties, against 5 FU-induced gastrointestinal damage. Materials and methods: Wistar albino rats were divided into 3 groups; Control group, 5-FU group (30mg/kg/day on days 0, 2, 4), and 5-FU+SF (30 mg/kg/day 5-FU on days 0, 2, 4 + 600 mg/kg/day SF for 14 days). At the end of the experiment, stomach and intestinal tissue samples were collected and immunohistochemically iNOS, caspase-3, CD4+ and CD8+ were measured. Besides, structural damage was assessed with hematoxylin-eosin and caspase-3 and 9 activities were evaluated using western blot analysis. Results and Discussion: It was determined that iNOS, caspase-3, caspase-9 activities, CD4+ and CD8+ levels and structural damage significantly increased in both stomach and intestinal tissues. Furthermore, elevated markers were regressed almost to control levels in SF administrated group. Conclusion: SF may have an ameliorative effect, thus reducing the gastrointestinal damage caused by 5 FU. More clinical and scientific research should be conducted as the silk fibroin may be a suitable candidate against the adverse effects of chemotherapeuic agents. [ABSTRACT FROM AUTHOR]

Purpose: In the presence of acute or chronic inflammation in the periapical tissues caused by various anaerobic and facultative bacteria, it is aimed to create suitable healing conditions by performing successful root canal treatment. However, endodontic flare-ups may occur between appointments, and this may cause discomfort for the patient and damage the patient-clinician relationship. Therefore, in this brief review, it is aimed to describe the possible preventive effects of the natural medicine Pelargonium sidoides extract (EPs® 7630), which has broad anti-infective and anti-inflammatory properties. Methods: PubMed and Google Scholar databases were searched and reviewed related to P. sidoides. The anti-inflammatory and antimicrobial effects of P. sidoides extract and its chemical constituents in periodontitis and other systemic infections are discussed. Results: Clinical and in vitro studies have confirmed that P. sidoides extract and some of its fractions may be involved in inflammatory tissue responses by showing immunomodulatory effects in mild infections of periapical tissues. This implies that the natural remedy, EPs® 7630, could be a potential therapeutic and prophylactic medicine for root canal treatments. Conclusion: This review provides basic information about the immunomodulatory, anti-infective, and anti-inflammatory effects of EPs® 7630 and outlines its possible functions in periradicular tissues as a promising therapeutic medicine. [ABSTRACT FROM AUTHOR]

The purpose of the study was to investigate the therapeutic effects of α‐lipoic acid (ALA) on an induced‐acute pulpitis model in rats. Twenty‐four Wistar albino rats were randomly divided into three groups: control, induced‐acute pulpitis (PULP) and PULP + ALA groups. In the PULP and PULP + ALA groups, the crowns of the maxillary left incisors were removed horizontally. All exposed pulp tissues were treated with 5 µL LPS solution. In the PULP + ALA group, the rats were treated intraperitoneally with a single dose of ALA (100 mg/kg). The rats were sacrificed 24 h after pulp injury, and the trunk blood and pulp samples were collected and then determined using ELISA assay kits. TNF‐α, IL‐1β, MMP‐1 and MMP‐2 levels in the serum and pulp tissues were considerably higher in the PULP group than the control group (p < 0.01–0.001). In the PULP + ALA group, TNF‐α, IL‐1β, MMP‐1 and MMP‐2 levels in the serum and pulp tissues decreased significantly compared to the PULP group (p < 0.05–0.001). ALA decreases pro‐inflammatory mediators and proteolytic enzymes, which might relieve acute inflammation. [ABSTRACT FROM AUTHOR]

Copyright of Türkiye Klinikleri Journal of Veterinary Sciences is the property of Turkiye Klinikleri and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective(s): Ischemia-reperfusion injury is a life-threatening clinical problem that can occur after transplantation or a number of clinical procedures. The purpose of the study was to investigate the effects of Ambroxol on kidney damage caused by experimentally induced ischemia-reperfusion injury in rats. Materials and Methods: Wistar albino rats were divided into 3 groups: Control (CTR, n=6), Kidney ischemia-reperfusion (K-IR, n=6), And kidney ischemia reperfusion+Ambroxol (K-IR+AMB, n=6). In K-IR+AMB group, Ambroxol (30 mg/kg) was administered orally 30 min before the ischemia period. K-IR and K-IR+AMB groups underwent 45 min of kidney ischemia followed by a 6-hour reperfusion period. At the end of the reperfusion period, blood and kidney tissue samples were collected after euthanasia. From the blood samples, BUN and creatinine levels were determined to assess kidney function, and TNF-α and IL-1β concentrations were evaluated to determine inflammatory response. Results: While serum BUN, creatinine activities, and TNF-α and IL-1β concentrations were higher in both IR groups compared with the CTR group, these values were found to be lower in the K-IR+AMB group compared with the K-IR group. Histopathological examination revealed that interstitial edema and desquamation of tubular cells in the K-IR group were more severe than in the K-IR+AMB group. Conclusion: Ambroxol treatment alleviated the production of pro-inflammatory cytokines and the harmful cellular effects in the tubular cells. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Faculty of Pharmacy of Ankara University / Ankara Üniversitesi Eczacilik Fakültesi Dergisi is the property of Ankara University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cholestasis is associated with the accumulation of bile acids and bilirubin in the hepatocytes and leads to liver injury. Pregnane X Receptor (PXR) coordinates protective hepatic responses to toxic stimuli, and this receptor was reported to stimulate bile secretion by increasing MRP2 expression. Since PXR activators were reported to be anti-inflammatory in the liver, PXR was proposed as a drug target for the treatment of chronic inflammatory liver diseases. We investigated the potential protective effect of spironolactone (SPL), an enzyme inducer, in hepatotoxicity induced by bile duct ligation in rats. Wistar Albino (250-300 g) rats were divided into the control group and the bile duct ligated (BDL) group. BDL group was divided into three subgroups; following BDL, for 3 days, the first group received propylene glycol (vehicle of SPL) (blinded), the second subgroup received spironolactone (SPL) (200 mg/kg oral), and the third subgroup received SPL for 3 days, starting 3 days after the bile duct ligation, in order to investigate if it has a healing effect after hepatitis had developed. The control group was sham-operated and received saline. At the end of the experiment, blood and tissue samples were collected. Serum TNF-a, NFĸB, bilirubin, IL-6 levels, ALT, AST, ALP activities and tissue MPO activity and oxidant damage increased after the bile duct ligation was significantly decreased following SPL administration. PXR and MRP2 activity showed an increase in the hepatocytes as a result of the treatment. In conclusion, it was observed that SPL administration significantly decreases liver inflammation and damage related to BDL. [ABSTRACT FROM AUTHOR]

The solute carrier (SLC) superfamily is one of the major sub-groups of membrane proteins in mammalian cells. The solute carrier proteins include more than 400 different membrane-spanning solute carriers organized with 65 families in the human. In solute carrier family neurons, neurotransmitter is considered to be a pharmacological target of neuropsychiatric drugs because of their important role in the recovery of neurotransmitters such as GABA, glutamate, serotonin, dopamine and noradrenaline and regulation of their concentration in synaptic regions. Therefore, solute carrier transporters play vital and different roles in neurodegenerative disorders. In this article, the role of solute carrier transporters in neurodegenerative disorders such as Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, Parkinson's diseases, depression, post-traumatic stress disorder, dementia, schizophrenia, and Epilepsy reviewed and discussed to see how defects or absences in SLC transporter cause neurodegenerative disorders. In this review, we try to summarize what is known about solute carriers with respect to brain distribution and expression. The review summarizes current knowledge on the roles of solute carrier transporters in neurodegenerative disorders. [ABSTRACT FROM AUTHOR]