Beta-adrenergic receptors are involved in anxiety disorders and help regulate anxiety-like behaviors. The nucleus accumbens (NAc), an important brain structure for emotional regulation and learning, plays a crucial role in anxiety. However, limited research has addressed the specific contribution of the NAc - particularly its noradrenergic mechanisms - in anxiety. This study aimed to investigate the effects of administering different doses of Xamoterol, a partial β1-adrenergic agonist, directly into the NAc shell, to understand its impact on anxiety-related processes and the retrieval of emotional memory. Forty adult male Wistar rats were bilaterally implanted with cannulas targeting the NAc shell. The rats received intra-accumbal Xamoterol at doses of 0.01, 0.1, or 1 μg/1 μl (saline). Five minutes after drug administration, anxiety-like behavior was tested using the Elevated Plus Maze (EPM). Twenty-four hours later, an EPM retention test was conducted to assess emotional memory retrieval. In addition, an open-field test was used to measure spontaneous locomotor activity. One-way ANOVA results showed that intra-accumbal Xamoterol (0.1 and 1 μg) significantly decreased anxiety-like behavior on the EPM. Conversely, head-dipping behavior (a risk assessment measure) was significantly increased at 0.01 and 0.1 μg doses of Xamoterol, which can be interpreted as an anxiolytic effect. Furthermore, higher doses of Xamoterol (0.1 and 1 μg) led to better emotional memory performance compared to the control group. None of the Xamoterol doses produced any significant change in locomotor activity (open-field test). These results suggest that β1-adrenergic receptors in the NAc shell play a role in mediating anxiolytic behavior and enhancing emotional memory retrieval in adult male rats.

Behavioral paradigms used to study hippocampal place and time cells typically focus on the perception of either space or time in isolation, rather than the interaction between these two dimensions. To address this gap, we developed the Time-Place Maze (TPM)s, a novel behavioral apparatus designed to require rats to integrate their perception of both spatial and temporal cues to obtain a reward. The maze consists of a start box (it consist Time-door), a reward box, and two connecting bridges of differing lengths. At the beginning of the task, the time-door opens with one of two possible delays: either 0 seconds or 3 seconds. In The short delay (0s) the short path is open to reward, and in the longer delay (3s) the long path is open. The TPM protocol includes three sequential phases: training, screening, and the main experimental phase. During the training phase, rats underwent four daily sessions. In the final phase, each rat completed 100 randomized tests designed to assess integration of time and place information in decision-making. Six adults male Wistar rats (weighing 230 ± 20 g) were included in the training phase; four met the screening criteria and progressed to the main phase. On average, rats required 16.25 corrective interventions during training. In the main phase, success rates across 100 trials ranged from 73% to 82%. Importantly, the total number of corrections in the main phase was significantly associated with overall task success (p = 0.019). These findings support the feasibility and utility of the TPM in animal models. The task provides unique opportunities in behavioral neuroscience research.

Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling and right ventricular (RV) dysfunction, processes that are increasingly associated with disturbances in cellular metabolism. We investigated whether transplantation of exogenous mitochondria derived from bone marrow mesenchymal stromal cells, alone or combined with sildenafil, could improve mitochondrial homeostasis and attenuate cardiopulmonary remodeling in monocrotaline-induced PAH. Male Wistar rats were assigned to control (CTRL, n = 8) or PAH (n = 32) groups. Fourteen days after induction of PAH, animals were randomized to receive saline, sildenafil (20 mg/kg/day for 14 days), intravenous mitochondrial transplantation (100 μg, days 14 and 21), or combined therapy. On day 28, echocardiography, invasive measurement of RV systolic pressure (RVSP), pulmonary vascular histology, gene expression analyses (vimentin, VE-cadherin, and mitochondrial metabolism–related genes), and high-resolution respirometry were performed. All treatments significantly reduced RVSP compared with untreated PAH. Mitochondrial therapy, alone or combined with sildenafil, decreased arteriolar α-smooth muscle actin content, whereas endothelial–mesenchymal transition was attenuated only with combined treatment. Mitochondrial transplantation and sildenafil increased Complex I–dependent respiration, whereas Complex IV activity improved exclusively with mitochondrial therapy. Combined treatment reduced plasma IL-6 and IL-1β levels compared with PAH. Thus, mitochondrial transplantation, particularly when combined with sildenafil, improved RV function, limited pulmonary vascular remodeling, reduced plasma inflammatory markers, and changed key mitochondrial pathways in experimental PAH.

The paper focuses on materials characterization and in vivo biocompatibility tests of Ti–6Al–7Nb–0.3REE wt.% alloys (REEs—Y, Ce, La) for use as a promising material to produce personalized medical implants and shed light on possible toxicity effects of REE alloy microdoping. All alloys were produced by the electric arc melting method and characterized by scanning electron microscopy (SEM), optical microscopy (OM), energy-dispersive X-ray spectroscopy analysis (EDX), X-ray diffraction (XRD), true density analysis, micro- and nanoindentation methods, and reducing/oxidation melting techniques. True density of alloys increased in the following order: Ti−6Al−7Nb−0.3Y (4.4563 ± 0.1075 g/cm3) < Ti−6Al−7Nb−0.3Ce (4.7255 ± 0.2853 g/cm3) < Ti−6Al−7Nb−0.3La (4.8019 ± 0.0111 g/cm3). XRD analysis indicated that Ti–6Al–7Nb–0.3Y alloy consisted of single α–Ti phase in comparison with Ti–6Al–7Nb–0.3La (α–Ti to β–Ti = 82 to 18) and Ti–6Al–7Nb–0.3Ce (α–Ti to β–Ti = 90.5 to 9.5). The single-phase Ti–6Al–7Nb–0.3Y alloy had the finest α–Ti phase crystallites (22.32 nm); the larger α–Ti crystallites in the dual-phase Ti–6Al–7Nb–0.3Ce and Ti–6Al–7Nb–0.3La (30.77 nm and 29.83 nm, respectively) suggested the presence of the β–Ti phase (23.34 nm and 25.61 nm, respectively). REE microdoping of alloys changed the lattice volume (∆V): α–Ti phase—0.269% for Ti–6Al–7Nb–0.3Y, 1.799% for Ti–6Al–7Nb–0.3Ce, 0.595% for Ti–6Al–7Nb–0.3La; and β–Ti phase—0.334% for Ti–6Al–7Nb–0.3Ce, 0.670% for Ti–6Al–7Nb–0.3La. Nanohardness (H) and elastic modulus (E) increased in the following order: Ti−6Al−7Nb−0.3La (4.01 GPa and 135 GPa, respectively) < Ti−6Al−7Nb−0.3Y (4.39 GPa and 137 GPa, respectively) < Ti−6Al−7Nb−0.3Ce (4.67 GPa and 146 GPa, respectively). In vivo tests were conducted using 46 sexually mature male Wistar rats by means of skin implantation of samples with d = 11 mm and h = 1 mm. Our research shows that Ti–6Al–7Nb–0.3La alloy (Group 2) and Ti–6Al–7Nb–0.3Ce alloy (Group 3) induced sustained hepatotoxic and nephrotoxic effects. Ti–6Al–7Nb–0.3Y alloy induced a slight local inflammatory response; however, serum biochemical analysis suggested this effect was compensated.

CeA-projecting VTA Neurons Contribute to Alcohol Withdrawal-induced Anxiety-like Behavior in Male and Female Rats.

Aging heightens susceptibility to ischemia-reperfusion (IR) injury, complicating liver transplantation, while the nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain containing 3 (NLRP3) inflammasome drives IR- and aging-induced inflammation. Although the effects of melatonin (MLT) on IR or aging have been studied separately, its impact on NLRP3 inflammasome activation in age- related IR injury remains unclear. This study investigates the impact of aging on hepatic IR injury, evaluating MLT therapeutic potential. for mitigating age-related damage. Aged and young male Wistar rats underwent 60min of ischemia followed by 6-24h of reperfusion. MLT (1mg/100g body weight) was injected 30min before ischemia, 10min before reperfusion, and 2h after reperfusion. Liver injury, oxidative stress and inflammatory responses, and activation of the NLRP3 inflammasome pathway were evaluated. Aged livers exhibited exacerbated IR injury, marked by elevated transaminases levels, severe histopathological damage, increased oxidative stress and heightened inflammatory responses compared to young IR-injured rats. MLT treatment significantly alleviated liver injury, reducing oxidative stress and inflammatory markers expression. Aging-associated IR injury correlated with increased NLRP3 inflammasome activation and pyroptosis, evidenced by the upregulation of apoptosis-associated speck-like protein containing a CARD (ASC-1), caspase-1 cleavage, interleukin (IL)-1β maturation and increased Il18 and Gsdmd gene expression; while MLT treatment suppressed this activation, downregulating these markers in aged IR-injured livers. These findings highlight the efficacy of MLT in mitigating IR-induced liver damage in aged rats by inhibiting the NLRP3 inflammasome activation, supporting its potential as a therapeutic strategy for age-related liver dysfunction.

Sacubitril/valsartan is a combined neprilysin inhibitor/angiotensin II receptor blocker which simultaneously potentiates the beneficial effects of natriuretic peptides while blocking angiotensin II accumulation. Numerous studies suggest that sacubitril/valsartan has better renal protective effects compared to valsartan but the evidence remains inconsistent. This study compared renal and blood pressure (BP)-lowering effects of sacubitril/valsartan versus valsartan in rats with adenine-induced chronic kidney disease (CKD). This model replicates slow progression and structural and functional characteristics of human CKD. Male Wistar rats (n = 24) were divided into four groups and treated for 35 days as follows: group 1 served as control; group 2 received 0.25% adenine; group 3 received adenine plus sacubitril/valsartan; group 4 received adenine plus valsartan. Adenine significantly increased systolic BP. It also significantly increased the urinary albumin/creatinine ratio, N-acetyl-β-D-glucosaminidase (NAG), plasma urea, creatinine, uric acid, and neutrophil gelatinase-associated lipocalin (NGAL) while reducing creatinine clearance. Additionally, adenine significantly increased inflammatory markers, decreased antioxidant activity, and induced tubular necrosis, dilatation, and interstitial inflammation. Sacubitril/valsartan significantly reduced systolic BP, with greater effects than valsartan. Both treatments reversed adenine-induced alterations in urinary albumin/creatinine ratio, NAG, plasma urea, creatinine, NGAL, and creatinine clearance, with more pronounced improvements in urea, NAG, and creatinine clearance observed with valsartan. Furthermore, both treatments ameliorated inflammatory and antioxidant changes to a comparable extent. Both treatments showed histopathological improvements, but these were more marked with valsartan. To conclude, both sacubitril/valsartan and valsartan effectively mitigated adenine-induced CKD changes, with sacubitril/valsartan producing greater systolic BP reduction and valsartan showing more pronounced renoprotective effects.

Relevance. Animals with knockout of the dopamine transporter gene (DAT–KO) reproduce the main symptoms of attention deficit hyperactivity disorder (ADHD). Changes in DAT function in DAT-KO rats are a key mechanism in various pathological conditions associated with hyperdophaminergia. The aim of this study was to investigate the features of the manifestation of behavior patterns in response to novelty in free behavior in DAT-KO rats compared with heterozygous animals for the knockout gene (DAT-HET) and wild-type (WT) rats Methods. The experiments were conducted on 57 male Wistar rats DAT-KO, DAT-HET and WT. Rats with a knockout of the DAT gene were initially obtained from St. Petersburg State University, the Institute of Translational Biomedicine. Genotyping and behavior research in the open field were carried out. The analysis of behavior patterns was used: locomotion; sniffing; rearing; grooming; movement in place (changing the coordinates of the head and body within a conditional circle, the center of which is the relatively stationary hind limbs of the animal); peering into the hole; stand on the wall (rearing with an emphasis on the wall of an open field). Results. The DAT-KO rats showed marked hyperactivity compared to the WT and DAT-HET rats, they spent less time in the center of the field and moved in a repetitive circular pattern along the walls. The manifestations of investigatory activity in DAT-KO rats decreased in the number of peering into the hole and sniffings compared with WT and DAT-HET rats. The manifestations of anxiety in DAT-KO rats decreased in the number of acts of "grooming" and movements in place. In DAT-HET rats, there was an increase in locomotor and investigatory activity compared with WT. Conclusion. Based on the analysis of their own behavioral data and other studies, it is concluded that behavioral disinhibition is an overlapping feature of the elements of addictive behavior: impulsivity and compulsivity, which require independent study in DAT-KO animals. The presence of hyperdophaminergia, increased locomotions and investigations in DAT-HET rats with simultaneous cognitive impairment can predict addictive behavior disorders under conditions of gene-environment interaction.

Background: Diabetes mellitus-induced hyperglycemia triggers oxidative stress, characterized by elevated malondialdehyde (MDA) and impaired catalase (CAT) activity. Stevia rebaudiana, rich in steviol glycosides and polyphenols, demonstrates promising antioxidant properties, yet systematic dose-response data on oxidative stress biomarkers remain limited. Objectives: To evaluate the dose-dependent effects of stevia leaf extract on serum MDA levels and CAT activity in alloxan-induced hyperglycemic rats. Methods: Twenty-five male Wistar rats were allocated into normal control, diabetic control (alloxan 120 mg/kg), and three treatment groups receiving alloxan plus stevia extract at 100, 200, or 400 mg/kg body weight orally for 14 days (n=5/group). Serum MDA and CAT were measured spectrophotometrically. Results: Diabetic control showed significantly elevated MDA (2.68±0.62 mg/dL) versus normal control (1.78±0.30 mg/dL). Stevia extract dose-dependently reduced MDA: 1.70±0.19, 1.54±0.20, and 1.38±0.09 mg/dL at 100, 200, and 400 mg/kg, respectively, representing 36.6%, 42.5%, and 48.5% reduction. The 400 mg/kg dose achieved MDA levels comparable to normal control. CAT activity showed dose-dependent restoration trend (7.92±0.76 to 8.58±0.52 mg/dL). Conclusion: Stevia leaf extract (400 mg/kg BW) effectively reduces oxidative stress in hyperglycemic rats through significant dose-dependent MDA reduction, with potential catalase benefits requiring further investigation.

Background Vestibular disorders, particularly Ménière’s disease, represent significant neurological conditions affecting balance, spatial orientation, and quality of life. While endolymphatic hydrops is recognized as the pathological hallmark of Ménière’s disease, the relationship between thyroid dysfunction and vestibular pathology remains incompletely understood. Clinical observations suggest associations between hypothyroidism and vestibular symptoms, yet experimental evidence demonstrating causality is lacking. Objective To investigate whether surgically-induced hypothyroidism causes endolymphatic hydrops development in an experimental rat model and to characterize the histopathological changes in vestibular structures. Methods Twelve male Wistar albino rats were randomly allocated to total thyroidectomy ( n = 4), sham surgery ( n = 4), and control ( n = 4) groups. Thyroid function was assessed via serum thyroid-stimulating hormone (TSH) and thyroxine (T4) measurements at baseline and postoperative day 15. Animals were euthanized at 28 days post-surgery for comprehensive histopathological examination of temporal bones. Endolymphatic hydrops was evaluated using standardized semiquantitative scoring systems for Reissner’s membrane, vestibular structures, stria vascularis, and utricular macula. Results Thyroidectomized rats developed significant biochemical hypothyroidism with elevated TSH (mean difference: 0.378 μIU/mL, 95% CI: 0.183–0.573, p = 0.021) and decreased T4 levels (mean difference: −2.357 pmol/L, 95% CI: −3.521 to −1.193, p = 0.021). Histopathological examination revealed universal development of endolymphatic hydrops in all thyroidectomized animals (100% vs. 0% in controls, p < 0.001), affecting Reissner’s membrane, vestibular apparatus, stria vascularis, and utricular macula with varying severity. Conclusion This study provides the first direct experimental evidence that thyroid hormone deficiency induces endolymphatic hydrops in all examined vestibular structures. These findings establish a mechanistic link between hypothyroidism and vestibular pathology, with important implications for the neurological evaluation and management of patients presenting with vestibular symptoms and comorbid thyroid dysfunction.

Chlorfenapyr (CFP) is an insecticide known to induce hepatotoxicity through oxidative stress, inflammation, and mitochondrial dysfunction. Resveratrol (RES) exhibits antioxidant and anti-inflammatory properties, and its delivery via chitosan nanoparticles (RES-CNPs) may enhance its protective effects. This study aimed to investigate the hepatoprotective potential of RES and RES-CNPs against CFP-induced liver damage in Wistar rats. Sixty male Wistar rats were randomly divided into six groups (n = 10): control, RES, RES-CNPs, CFP, CFP + RES, and CFP + RES-CNPs. Treatments were administered orally for 30 days. Liver function, lipid profile, oxidative stress markers, antioxidant defense system, energy metabolism, mitochondrial function, inflammatory gene expression, histopathology, and ultrastructure were evaluated exposure significantly decreased total protein, albumin, antioxidant levels (GSH, CAT, SOD, GPX), ATP, and PDH activity, while increasing liver enzymes (AST, ALT, ALP), lipid peroxidation (MDA, PCO), mitochondrial dysfunction, inflammatory gene expression (NF-κB, TNF-α, IL-6), CRP, and total leukocyte count (p < 0.05). Co-administration of RES-CNPs significantly restored these biochemical, molecular, and histological parameters, showing superior efficacy to crude RES in most endpoints and achieving values close to the negative control for several markers (p > 0.05). Histopathological and ultrastructural analyses confirmed CFP-induced hepatocyte degeneration and necrosis, which were ameliorated by RES-CNPs, with near-normal liver architecture and cellular integrity. RES-CNPs effectively mitigate CFP-induced hepatotoxicity by restoring liver function, enhancing antioxidant defenses, preserving mitochondrial function, and suppressing inflammation. RES-CNPs demonstrated superior hepatoprotective effects compared to crude RES, highlighting their potential as a therapeutic strategy against xenobiotic-induced liver injury.

Current clinical guidelines recommend withholding renin-angiotensin-aldosterone system (RAAS) inhibitors during acute kidney injury (AKI) due to concerns over impaired glomerular perfusion. However, their potential to mitigate post-AKI inflammation and fibrosis remains unexplored. We hypothesized that telmisartan, an angiotensin II receptor blocker (ARB) with reported PPAR-γ activity, would enhance recovery from ischemic AKI. Male Wistar rats were subjected to unilateral nephrectomy and 45-minute ischemia in the contralateral kidney, or sham surgery. Animals were randomized to receive telmisartan (3 mg/kg/day) or placebo for 10 days, starting one week before injury. Telmisartan treatment significantly accelerated the recovery of renal function and attenuated tubular necrosis, inflammation, and the expression of injury biomarkers. At the whole‑kidney tissue level at 72 h post‑IRI, bulk RNA‑sequencing compared to healthy control mice without IRI revealed apparent broad metabolic dysfunction, with suppression of fatty acid oxidation and mitochondrial pathways, which may reflect both injury‑driven changes in cellular composition and transcriptional regulation within surviving cells. These transcriptomic findings 72 h after IRI were significantly blunted or even abolished by telmisartan. This treatment effects did not show evidence of direct PPAR-γ pathway activation, This study suggests that the metabolic modulatory effects of certain angiotensin II receptor blockers may provide therapeutic benefit during the recovery phase of AKI, independent of direct PPAR-γ signaling.

Background Cisplatin (CIS) is a highly effective chemotherapeutic agent widely used to treat solid tumors. However, its clinical use is significantly limited by dose-dependent hepatotoxicity, characterized by hepatocellular injury and apoptosis. Despite extensive research efforts, an effective pharmacological strategy to reduce CIS-induced liver dysfunction remains elusive. Sacubitril/valsartan (VS), an angiotensin receptor–neprilysin inhibitor, has shown cytoprotective and anti-apoptotic effects in various models of organ toxicity. However, its ability to protect against CIS-induced liver damage has not been thoroughly studied. This research aimed to assess the hepatoprotective potential of VS in rat models of cisplatin-induced liver toxicity, focusing on oxidative markers including reactive oxygen species (ROS) and malondialdehyde (MDA), as well as the roles of caspase-3 inhibition and modulation of retinoid X receptor-alpha (RXR-α) in its mechanism. Methods In this study, adult male Wistar rats were randomly assigned to four groups: control, VS-treated, cisplatin-treated, and CIS + VS co-treated. Hepatotoxicity was induced by administering cisplatin at 8 mg/kg via intraperitoneal injection, repeated over three cycles. Meanwhile, VS was given orally at 60 mg/kg daily for 10 days. Liver biochemical markers, including ROS, MDA, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total protein (TP), albumin (ALB), total bilirubin (TBIL), and lactate dehydrogenase (LDH), were measured using ELISA. Liver tissue was examined histologically with hematoxylin and eosin staining, and the expression of caspase-3 and RXR-α was evaluated through immunofluorescence. Results Cisplatin administration significantly increased ROS, MDA, ALT, AST, ALP, TBIL, and LDH levels, while decreasing TP and ALB, indicating severe liver dysfunction. Histopathology showed extensive hepatocellular degeneration, necrosis, and inflammation. Co-treatment with VS significantly normalized liver function tests, improved protein levels, and maintained normal liver histology. Additionally, VS markedly reduced caspase-3 immunoreactivity while increasing RXR-α expression compared to CIS alone. Conclusion Sacubitril/valsartan appears to protect the liver from cisplatin toxicity, primarily by inhibiting oxidative stress and apoptosis through caspase-3 suppression, and modulating RXR-α signaling. These results provide new insights into the mechanisms involved and suggest that VS may be a promising adjunct therapy to lessen cisplatin-induced hepatotoxicity during chemotherapy.

This study aimed to evaluate the effects of N-acetylcysteine (NAC) supplementation in apical periodontitis (AP) induced in rats. Eighteen male Wistar rats were randomly assigned to three groups: control, AP, and AP plus NAC. NAC was administered by oral gavage (100 mg/kg/day), beginning 1 day after lesion induction and continued daily until the day preceding euthanasia. AP induction was performed by exposing the dental pulp of the lower first molars bilaterally, maintaining this condition for 28 days. After this period, the animals were euthanized, and the following biological materials were collected: blood (for systemic oxidative stress analysis) and hemimandibles for histopathological and histochemical, and micro-computed tomography analyses, aiming to measure bone quality parameters and periapical volume. Statistical analyses were performed using one-way ANOVA and Tukey's post hoc test. In addition, correlation analyses and multivariate analyses of variance (MANOVA) were performed on the biochemical parameters. The study results showed that animals supplemented with NAC had greater preservation of bone quality parameters and a reduction in periapical volume progression when compared to the only apical periodontitis group. Additionally, in the analysis of systemic oxidative stress, supplemented animals showed higher antioxidant parameter levels and lower oxidant levels compared to non-supplemented animals, which also showed reduced preservation of bone collagen content. The study findings suggest that NAC supplementation promoted greater preservation of bone quality, reduced periapical volume development, and modulation of endogenous antioxidant and oxidant aspects. This indicates that NAC can decrease local and systemic damage caused by AP, highlighting its potential as an adjunctive agent in processes involving systemic oxidative stress and the preservation of biological structures.

Abstract Purpose The aim of the present study was to investigate the effects of an HIIT protocol on the bone mineral density (BMD), mechanical strength, and bone mineralization of animals supplemented with creatine. Methods Forty male Wistar rats, 60 days old, were used. The animals were divided into four groups: (1) control (C), (2) creatine (Cr), (3) training (T), and (4) training + creatine (TCr). The animals in the Cr and TCr groups were supplemented with creatine monohydrate (2% of daily feed weight). The T and TCr groups performed an HIIT protocol, 5x/week, for 12 weeks, with the treadmill at a 15° inclination. The running protocol was performed at 60% of the Vmax obtained in the maximum effort test for 3 min, followed by 4 min of running at 85% of the Vmax. At the end of the experiment, the animals were euthanized, and samples of the tibia were collected. Subsequently, bone densitometry analyses were performed to determine the BMD and Raman spectroscopy to observe bone mineralization. The three-point mechanical test was also used to determine bone strength (Fmax). Results The results showed a reduction in the TCr group for mechanical strength (Cr vs TCr) and for the analyzed minerals (C vs TCr) ( p &lt; 0.05). Conclusion HIIT added to creatine supplementation led to decreases in mechanical strength and the mineralization of the tibia.

Fever, or pyrexia, is defined as an elevation in body temperature beyond normal physiological limits and pain an unpleasant sensory and emotional experience occur in some types of fever. Dioscorea bulbifera leaves are traditionally used for managing fever with aches and pain as per Siddha Literature. Based on these traditional claims, the present study aimed to scientifically evaluate the antipyretic and analgesic activities of Diacorea bulbifera leaf decoction using experimental animal models. For antipyretic activity, 18 male Wistar albino rats were divided into three groups: control, standard, and test. Fever was induced using 15% w/v Brewer's yeast administered subcutaneously. After 18 hours, rectal temperatures were recorded at 30, 60, 90, and 120 minutes following treatment. The control group received 1 ml/kg normal saline, the standard group received paracetamol syrup, and the test group received Diacorea bulbifera leaf decoction according to standard dose calculation. For analgesic activity, 18 female Wistar albino rats were divided similarly, and the tail immersion method was used. Tail withdrawal times were recorded at 30, 60, 90, and 120 minutes after administering saline, diclofenac and diascorea bulbifera decoction. The Dioscorea bulbifera decoction significantly reduced fever, showing effects comparable to paracetamol after 90 minutes. It also exhibited notable analgesic activity from the 60th minute onward, with stronger and longer-lasting effects than diclofenac. Dioscorea bulbifera leaf decoction demonstrates significant antipyretic and analgesic effects, supporting its traditional use in treating fever and pain.

Effect of Carica Papaya (Paw-Paw) Leaf Extract on the Histology of the Pancreas in the Tramadol-Induced Male Wistar Rats

Background Osteoarthritis (OA) is the most common form of arthritis affecting the elderly and obese population, and requires long-term medical management. Inflammatory pathways, possibly initiated by tissue damage and stress are involved in the pathogenesis of OA. Citrus medica Linn., known for its anti-inflammatory and analgesic properties, has been the focus of management of OA in recent years. Purpose To explore the therapeutic potential of Citrus medica gel in Wistar Albino rat OA model with standard Aceclofenac gel. Materials and Methods An experimental interventional animal study was conducted in which OA was induced in 24 male Wistar Albino rats (12-week-old) using monosodium iodoacetate. The animals were observed for 1 week for signs of joint inflammation. They were then divided into four groups. Group A (standard) received Aceclofenac gel twice daily (BD) for 4 weeks. Group B received C. medica gel (0.2 g, 0.33% w/w) once daily (OD). Group C received C. medica gel (0.2 g, 0.33% w/w) BD, and Group D was kept as a disease control throughout the study. The results were compared between groups using one-way analysis of variance (ANOVA). Results The double-dose C. medica gel regimen displayed a significant and earlier reduction in ankle joint circumference (ANOVA, p value &lt; .001). Pain relief was observed, as evidenced by a favorable reversal of the arthritic index and score compared to the standard treatment. Conclusion This study highlights the potential of C. medica gel in reducing inflammation and pain associated with OA. These findings warrant further investigation through clinical trials.

Dictyota ciliolata ameliorates hyperglycemia, oxidative stress, and inflammation via modulation of metabolic and signaling pathways in diabetic rats.

MDMA and psilocybin regulate oligodendrocyte-lineage cell numbers and anxiety-like behaviors in a rat model of fear.