Aim: Breast cancer is a common disease in women with high morbidity and mortality. Although various treatment modalities are available, chemoresistance remains a major problem in breast cancer. This study aimed to investigate the interactions of lecanoric acid, a natural compound with bioactive properties, with receptors considered therapeutic targets in breast cancer.Materials and Methods: The 3D structures of the target proteins 17β-HSD1 (1FDW), ERα (6CBZ), EGFR (1M17), and Bcl-xL (2W3L) were retrieved from the RCSB Protein Data Bank (RCSB PDB; https://www.rcsb.org) using their PDB IDs. The 3D structure of lecanoric acid was downloaded from the PubChem database and prepared for analysis. AutoDock Vina was used for molecular docking analyses. Ligand-receptor interactions were visualized using Discovery Studio 2021 (BIOVIA, USA). In addition, the physicochemical, medicinal chemistry, pharmacokinetic, and toxicity profiles of lecanoric acid as a drug candidate were comprehensively evaluated using ADMETlab 3.0.Results: Molecular docking analyses indicated that lecanoric acid bound to the target proteins with docking scores ranging from -7.1 to -7.7 kcal/mol. In addition, the probability of P-gp inhibition by lecanoric acid was predicted to be very low, and the radar plot showed that the evaluated ADMET parameters remained within the predefined lower and upper limits.Conclusions: Lecanoric acid was found to exhibit notable binding affinity toward 17β-HSD1, ERα, EGFR, and Bcl-xL, which are of critical importance in breast cancer pathology. Although lecanoric acid appears to have important advantages in terms of its physicochemical, medicinal chemistry, pharmacokinetic, and toxicity profiles, in vitro and in vivo studies are needed to validate its therapeutic potential.

Parkinson’s disease (PD), the second most common neurodegenerative disorder, is characterized by α-synuclein aggregation and loss of dopaminergic neurons, and current treatments are symptomatic. Multiple intricate mechanisms contribute to the pathogenesis, and the effectiveness of single-target approaches is therefore limited. Current approaches highlight therapeutic candidates capable of simultaneously modulating multiple pathways. Recent clinical and experimental studies of sodium-glucose cotransporter inhibitors (SGLT2is), approved for the treatment of type 2 diabetes mellitus, have indicated their pleiotropic and neuroprotective potential. SGLT2i dapagliflozin has several features, including low molecular weight, blood-brain barrier permeability, and tolerability. This study investigated the effects of dapagliflozin on pathways implicated in the pathogenesis of PD in a 6-hydroxydopamine-induced experimental PD model in female Sprague-Dawley rats using in silico, histopathological, immunohistochemical, and biochemical methods. Dapagliflozin was administered by oral gavage at four different doses (2.5 mg/kg, 5 mg/kg, 7.5 mg/kg, and 10 mg/kg) for 14 days. Motor deficits were evaluated by means of behavioral tests, and dapagliflozin was observed to alleviate motor dysfunction. Tyrosine hydroxylase expression increased in brain tissues, whereas A2AAR, TNF-α, and APAF-1 levels, as well as α-synuclein and caspase-3 expression, decreased. In molecular docking analyses, dapagliflozin showed notable binding affinity to PD-associated human target receptors. Our results suggest that dapagliflozin may exert potential neuroprotective effects via modulation of inflammatory, oxidative stress-related, and apoptosis-associated pathways and may represent a promising repurposing candidate for PD.

Neuropathic pain is a chronic condition characterized by central sensitization (CS) and inadequacy of current treatments. Although antipsychotics are considered potential adjuvant treatments, they are generally treated as a homogeneous class, and their specific anti-nociceptive mechanisms remain unclear. This study challenges the assumption that antipsychotics exhibit a uniform class effect by comparing the effects of five commonly used antipsychotics on key central sensitization pathways.A paclitaxel-induced neuropathic pain model was established in rats. After model stabilization, antipsychotic treatments were administered orally for 14 days. Mechanical nociception was assessed with the Randall-Selitto test and locomotor activity with the open field test. Protein and mRNA expression of targeted pathways in the M1 cortex and spinal cord were examined by immunohistochemistry and in situ hybridization.All five antipsychotics significantly reduced mechanical hyperalgesia without causing sedation. However, each agent exhibited a distinct molecular "fingerprint": Quetiapine and chlorpromazine strongly suppressed the expression of phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphorylated GluN2B (p-GluN2B) in both the cortex and spinal cord. Haloperidol and aripiprazole exerted their effects primarily by modulating the sigma-1 receptor in the spinal cord. Risperidone, despite exhibiting anti-hyperalgesic effects, had the weakest and most paradoxical effects on the pathways examined.Our findings reveal that antipsychotics exhibit significant mechanistic heterogeneity in neuropathic pain modulation. A "one-size-fits-all" approach is therefore inadequate for this drug class. Understanding each agent's unique mechanistic profile could inform the development of targeted and more effective treatment strategies tailored to the patient's pathophysiology.

Objective: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease in which multiple mechanisms play a role in its pathogenesis. However, no radical treatment is currently available for the disease. The potential for repositioning of the antidiabetic drug empagliflozin, which has been reported to have neuroprotective effects in recent studies, in ALS was investigated using computational models.Methods: In this study, to identify ALS-related target proteins, protein–protein interaction networks and disease–gene enrichment analysis were constructed using the STRING database. For molecular docking analyses, the 3D structures of these ALS-associated receptors SOD1 (2C9V), hnRNP A1 (1HA1), TDP-43 (4BS2), SQSTM1/p62 (5YP7) were obtained from the RCSB Protein Data Bank. Empagliflozin and the receptors were prepared using UCSF Chimera v1.19 and AutoDockTools 1.5.7, and binding scores were recorded with AutoDock Vina. The ADMET properties of empagliflozin were determined using ADMETlab 2.0 and LogBB_Pred.Results: In the protein networks generated by STRING, ALS-related proteins with high confidence scores and physical interactions were identified, and among them, four target proteins showing significant interactions and with available PDB codes were selected. Molecular docking analyses revealed that empagliflozin exhibited moderate-to-high binding interactions with SOD1 (-8.5 kcal/mol), TDP-43 (-7.7 kcal/mol), hnRNP A1 (-7.3 kcal/mol), and SQSTM1/p62 (-7.1 kcal/mol). According to ADMET analysis, empagliflozin can cross the blood–brain barrier, has a low risk of hepatotoxicity, and shows potential interactions with androgen receptor and aromatase.Conclusion: In this study, conducted to repurpose empagliflozin via ALS-related mechanisms, which has been reported to have cardioprotective, hepatoprotective, and renoprotective effects in clinical studies, the findings obtained using computational models suggest that empagliflozin may have neuroprotective effects in ALS.

This study presents the wound healing supporting processes of cream formulations developed using Plantago lanceolata L. (PL) methanol extract in rats with full-thickness excisional skin wounds. Following the creation of full-thickness excisional skin wounds in rats, these formulations (25 mg/g, 50 mg/g, and 100 mg/g) and Fito cream (control drug) were applied topically to the wound areas for 14 days. Biochemical (TNF-alpha, IL-8, MMP-2), histopathological, and immunohistochemical (FGFR2/Bek, IGF-I, TGF-beta 1, VEGFR2, ERK 1/2, and iNOS) analyses were performed on wound tissues following sacrifice. Major components of the PL methanol extract were determined by LC-HRMS analysis. Interactions between major components and inflammation-associated human receptors were evaluated using molecular docking (Schrodinger Maestro version 13.9.138.) methods. Significantly greater closure of wound areas was observed on day 14 in the rats treated with the developed new cream formulations and Fito cream compared to the positive control group. Inflammation was significantly lower, and epithelialization was higher in the group treated topically with 100 mg/g PL methanol extract-containing cream formulation than in the other groups. Additionally, the major components of the PL methanol extract exhibited strong binding affinity with inflammation-related human receptors. The study findings show that the developed cream formulation supports wound healing by regulating antioxidant and anti-inflammatory pathways. The PL cream formulation (100 mg/g) was more effective in wound healing than Fito cream and possesses significant potential for clinical use.

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with liver dysfunction and remains a major cause of mortality among patients with advanced liver disease. This study aimed to evaluate the protective effects of Pycnogenol in a rat model of thioacetamide-induced hepatic encephalopathy. Thirty-two rats were assigned to four groups: control, HE (TAA), and two treatment groups receiving Pycnogenol at 5 mg/kg and 10 mg/kg. HE was induced by intraperitoneal administration of TAA at 200 mg/kg for three consecutive days. Pycnogenol was administered orally for 14 days prior to and during TAA exposure. Behavioral tests (locomotor activity, elevated plus maze), histopathological evaluations, biochemical parameters, immunohistochemical staining, and gene expression analyses (qPCR) were performed. Pycnogenol administration resulted in significant improvements in locomotor activity, reductions in oxidative stress markers, and decreased expression of IL-1β, TNF-α, NF-κB, and caspase-3. Histopathological examination revealed alleviation of hepatic and neuronal degeneration. Immunohistochemistry confirmed reduced GFAP and iNOS staining in brain tissues. Pycnogenol demonstrated neuroprotective and hepatoprotective effects in this experimental model, likely through modulation of oxidative stress and inflammatory pathways. Although these findings highlight the potential translational relevance of Pycnogenol as a supportive strategy for hepatic encephalopathy, further studies in chronic models and clinical settings are required to confirm its therapeutic applicability.

Parkinson's disease is one of the most prevalent neurodegenerative disorders worldwide. The kynurenine pathway associated with oxidative stress and neuroinflammation is recognized to contribute to its pathophysiology, although the exact mechanism is not fully elucidated. In neuroinflammation, IDO-1 catalyzes the conversion of tryptophan to neurotoxic QUIN through the kynurenine pathway. Consequently, QUIN increases oxidative stress via nNOS and NMDA, which causes neurodegeneration. Few studies have reported on the effect of different antiviral drugs in Parkinson's disease; the exact mechanism is still unknown. The antiviral acyclovir has been shown to have neuroprotective properties and can cross the blood-brain barrier. We examined acyclovir's effects and potential mechanisms in the 6-OHDA-induced in vitro model of Parkinson's disease in SHSY5Y cells using biochemical, immunocytochemical, and in silico methods. MTT assay demonstrated that acyclovir significantly decreased cell mortality induced by the neurotoxic 6-OHDA at dosages of 3.2 mu M, 6.4 mu M, 12.8 mu M, 25.6 mu M, and 51.2 mu M. In immunocytochemical analysis, acyclovir treatment decreased alpha-synuclein and TNF-alpha expressions in cells. In biochemical analyses, while IL-17A and TOS levels decreased depending on varying doses (1.6 mu M, 3.2 mu M, 6.4 mu M, 12.8 mu M), TAC levels increased. Using in silico analyses to investigate the mechanism showed that acyclovir docked with TNF-alpha, IL-17A, IDO-1, nNOS, alpha-synuclein, and NMDA. The findings demonstrated that acyclovir had neuroprotective effects by modulating the kynurenine pathway and decreasing neurodegeneration via QUIN inhibition in an in vitro Parkinson's disease model. Although the

According to the journal rules, an abstract is not required for the Editorial article type.

OBJECTIVES:This study aims to evaluate the impact of tetracalcium phosphate (TTCP) applied directly to the fracture line in a rat femur fracture model. MATERIALS AND METHODS:Thirty-three male Sprague-Dawley rats weighing 350 to 400 g were randomly and equally divided into three groups: normal control (NC), fracture control (PC), and TTCP treatment group. Standardized femur fractures were created in the PC and TTCP groups and fixed using intramedullary Kirschner wires. In the TTCP group, TTCP dissolved in distilled water was applied directly to the fracture line. All rats were sacrificed on postoperative Day 28. Radiological, histopathological, and biochemical analyses were performed to assess fracture healing. RESULTS:Radiological scoring revealed significantly higher fracture healing in the TTCP group compared to the PC group on Days 14 and 28 (p<0.05). Histopathological analyses showed reduced inflammation and fibrosis, and increased chondrocyte activity and neovascularization in the TTCP group. On Day 28, serum tumor necrosis factor-alpha (TNF-α) levels were significantly higher in the PC group compared to TTCP and NC, while TTCP values were comparable to NC. No adverse tissue reactions were observed in any group. CONCLUSION:The TTCP enhances fracture healing when applied directly to the fracture line, without causing soft tissue irritation or histologically detectable adverse reactions. Its biological activity and ease of application suggest that TTCP may be a promising adjunct in the treatment of complex fractures.

Parkinson’s disease is a complex neurodegenerative disease that affects millions of people worldwide. The incidence and prevalence of Parkinson’s disease, the second most common neurodegenerative disease after Alzheimer’s disease, is gradually increasing. Although it is an important public health concern, the mechanisms related to Parkinson’s disease have not been fully elucidated. One of the main approaches to research on mechanisms and treatment related to Parkinson’s disease is the use of experimental models. In vitro and in vivo models enable the investigation of disease-related molecular and cellular processes and the testing of potential treatments. A variety of experimental models are used in Parkinson’s disease research, including toxin-induced models, genetic models, and transgenic models, each with their strengths and limitations. Experimental models come to the fore in research on Parkinson’s disease, which does not yet have a radical treatment. However, it is important to recognize that no experimental model truly represents all aspects of human Parkinson’s disease. For this reason, the findings obtained from the studies need to be supported by different test systems and interpreted carefully. Experimental models are invaluable in the quest to elucidate the mechanism of Parkinson’s disease and develop effective treatments.

BACKGROUND:Cisplatin is a potent anticancer agent widely employed in chemotherapy. However, cisplatin leads to toxicity on non-targeted healthy organs, including the liver. We investigated the hepatoprotective mechanism of arbutin (ARB), a glycosylated hydroquinone, against cisplatin-induced hepatotoxicity. METHODS:Rats were orally administered with ARB (ARB1 = 50 mg/kg; ARB2 = 100 mg/kg) for 14 consecutive days against hepatotoxicity induced by a single dose of cisplatin (10 mg/kg) on day 15. Three days after the intraperitoneal cisplatin injection, serum and liver tissue were collected for subsequent analyses. RESULTS:Cisplatin triggered marked increases in serum AST, ALT, and ALP activities, hepatic malondialdehyde (MDA) and reactive oxygen species (ROS) coupled with a considerable diminution in hepatic activities of superoxide dismutase (SOD), catalase (CAT) and the concentration of reduced glutathione (GSH). The gene expressions of interleukin-1β (IL-1β), tumor necrosis factor (TNF-α), and IL-6 were notably increased. The pre-administration of ARB1 and ARB2 reduced AST, ALT and ALP in serum and restored SOD, CAT, GSH, ROS, MDA and cytokine levels which was also evidenced by alleviated hepatic lesions. Further, cisplatin-induced prominent alterations in the gene expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), iNOS, NF-κB, Bax, Bcl-2, caspase-3 and 8-OHdG in the liver. Interestingly, ARB protected the liver and mitigated the cisplatin-induced alterations in serum AST, ALT, ALP, and reduced hepatic redox markers, 8-OdG, inflammatory markers and gene expressions. CONCLUSION:The findings demonstrate that ARB is a potential protective adjuvant against cisplatin-induced hepatotoxicity via inhibition of hepatic oxidative stress, inflammation, and apoptosis.

Background: Cisplatin is a potent anticancer agent widely employed in chemotherapy. However, cisplatin leads to toxicity on non-targeted healthy organs, including the liver. We investigated the hepatoprotective mechanism of arbutin (ARB), a glycosylated hydroquinone, against cisplatin-induced hepatotoxicity. Methods: Rats were orally administered with ARB (ARB1 = 50 mg/kg; ARB2 = 100 mg/kg) for 14 consecutive days against hepatotoxicity induced by a single dose of cisplatin (10 mg/kg) on day 15. Three days after the intraperitoneal cisplatin injection, serum and liver tissue were collected for subsequent analyses. Results: Cisplatin triggered marked increases in serum AST, ALT, and ALP activities, hepatic malondialdehyde (MDA) and reactive oxygen species (ROS) coupled with a considerable diminution in hepatic activities of superoxide dismutase (SOD), catalase (CAT) and the concentration of reduced glutathione (GSH). The gene expressions of interleukin-1 beta (IL-1 beta), tumor necrosis factor (TNF-alpha), and IL-6 were notably increased. The pre-administration of ARB1 and ARB2 reduced AST, ALT and ALP in serum and restored SOD, CAT, GSH, ROS, MDA and cytokine levels which was also evidenced by alleviated hepatic lesions. Further, cisplatin-induced prominent alterations in the gene expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), iNOS, NF-kappa B, Bax, Bcl-2, caspase-3 and 8-OHdG in the liver. Interestingly, ARB protected the liver and mitigated the cisplatin-induced alterations in serum AST, ALT, ALP, and reduced hepatic redox markers, 8-OdG, inflammatory markers and gene expressions. Conclusion: The findings demonstrate that ARB is a potential protective adjuvant against cisplatin-induced hepatotoxicity via inhibition of hepatic oxidative stress, inflammation, and apoptosis.

Agents that will accelerate wound healing maintain their clinical importance in all aspects. The aim of this study is to determine the antimicrobial activity of zinc oxide nanoparticles (ZnO NPs) ZnO nanoparticles obtained by green synthesis from Capparis spinosa L. extract and their effect on in vitro wound healing. ZnO NPs were synthesized and characterized using Capparis spinosa L. extract. ZnO NPs were tested against nine ATCC-coded pathogen strains to determine antimicrobial activity. The effects of different doses (0.0390625–20 µg/mL) of NPs on cell viability were determined by MTT assay. The effect of ZnO NPs doses (0.0390625 µg/mL, 0.078125 µg/mL, 0.15625 µg/mL, 0.3125 µg/mL, 0.625 µg/mL, 1.25 µg/mL) that increase proliferation and migration on wound healing was investigated in an in vitro wound experiment. Cell culture medium obtained from the in vitro wound assay was used for biochemical analysis, and plate alcohol-fixed cells were used for immunohistochemical staining. It was determined that NPs formed an inhibition zone against the tested Gram-positive bacteria. The ZnO NPs doses determined in the MTT test provided faster wound closure in in-vitro conditions compared to the DMSO group. Biochemical analyses showed that inflammation and oxidative status decreased, while antioxidant levels increased in ZnO NPs groups. Immunohistochemical analyses showed increased expression levels of Bek/FGFR2, IGF, and TGF-β associated with wound healing. The findings reveal the antimicrobial effect of ZnO nanoparticles obtained using Capparis spinosa L. extract in vitro and their potential applications in wound healing.

This chapter provides an overview of the industrial applications of essential oils, explaining their most common uses in various industries. Creative industries are constantly evolving with the use of novel, innovative and modern tools and ingredients towards more effective, safe, natural, and eco-friendly solutions to satisfy the demands and improve the well-being of the customers. Essential oils are natural, volatile, and complex compounds synthesized as secondary metabolites by plants. They are extracted from various parts of the plants, and determine the unique aroma, fragrance and flavor of the plant. Essential oils have a wide variety of chemical constituents such as terpenes, phenols, alcohols, esters, oxides, aldehydes, ketones, heterocycles, amines and amides. Depending on their major components, essential oils have many biological activities, mainly antimicrobial, antibiofilm, antioxidant, anti-inflammatory, analgesic, anesthetic, anti-proliferative, and insecticidal. This chapter focuses on the increased use of essential oils in the food, beverage, packaging, cosmetics, perfumery, medical, agriculture, textile and cleaning industries in line with the increasing awareness about the potential dangers of synthetic additives and the increasing demand of consumers for natural ingredients.

Products from Mentha species are widely used in medical applications, including wound healing, due to the bioactive compounds they may contain.However, data on the effect of Mentha longifolia L. on wound healing are limited.This study investigated the antimicrobial and wound healing-promoting effects of Mentha longifolia L. essential oil using in vitro methods.The chemical compositions of the essential oil were identified using gas chromatography/mass spectrometry, while the agar well diffusion and disk diffusion methods were used to determine antimicrobial activity against pathogenic strains.A scratch wound healing assay was performed following determination of the cytotoxic dose in human fibroblast cell lines.The media were used for biochemical analysis 48 h after the in vitro wound model.Immunohistochemical staining was applied to determine the contribution of the essential oil to wound healing.The essential oil exhibited varying levels of antimicrobial activity against the tested pathogens and increased cell viability.All doses in the scratch wound healing assay promoted wound closure in a shorter time than in the control group.TAC levels were higher in the treated groups than in the control group, while TOS, IL-6, and TNF-α levels were lower.Levels of expression of FGF 2, IGF, and TGF-β were higher in the treated groups than in the control group at increasing doses.The essential oil of Mentha longifolia L. exhibited antimicrobial effects and improved wound healing at doses of 5 µg/mL and 10 µg/mL.

Biofilms are defined as well-organized multicellular microbial communities attached to a surface and they are highly resistant structures to antimicrobial agents. The high resistance to conventional treatment techniques requires higher concentrations of antimicrobial agents to eradicate biofilm-forming bacteria. However, the harmful effects of high-dose antibiotics and disinfectant residues on human health have led to a shift in preferences toward the use of effective, safe, and environmentally friendly natural biofilm-fighting chemicals. In this chapter, the use of essential oils against biofilm-forming bacteria will be discussed. First, knowledge about definition, formation, and structural organization of biofilms will be gained. Then, the benefits of biofilms to microorganisms will be mentioned. In particular, the mechanisms of gaining resistance to antimicrobial agents will be covered in detail. Next, therapeutic approaches used to deal with biofilms will be briefly discussed. The following sections will provide an overview of the nature of essential oils, followed by further insight regarding the antimicrobial and antibiofilm activities of essential oils, their mechanism of action, and factors affecting their antimicrobial potential.

Abstract Objectives Bee venom is used for medicinal purposes, including the treatment of neurological and liver diseases, but its use as a primary health care approach for preventive purposes requires further exploration. The aim of this study was to provide the first investigation into the possible protective effects of bee venom against hepatic encephalopathy, a serious neurodegenerative disease. Materials and Methods An experimental animal study was conducted in which healthy albino Sprague–Dawley rats were randomized into three groups: healthy, control and bee venom groups. All rats were tested for locomotor activity at the beginning and end of the study. No intervention was made in the healthy group, whereas hepatic encephalopathy was induced in the control and bee venom groups by the administration of thioacetamide (TAA) (200 mg/kg/day). The bee venom group also received bee venom (5 mg/kg/day) subcutaneously every day for 14 days prior to the TAA administration. Results The results for the final locomotor activity tests were statistically better in the bee venom group than in the control group, supporting a beneficial effect of prophylactic bee venom application. Blood ammonia levels and liver weights, determined as indicators of inflammation, were lower in the bee venom group than in the control group and were close to levels in the healthy group, but not statistically significant. Conclusions Bee venom administration has protective effects against the development of hepatic encephalopathy and offers a promising therapeutic opportunity in preventive medicine.

In this study, we determined the therapeutic effect of parthenolide (PTL), the active component of Tanacetum parthenium, on neuropathic pain caused by paclitaxel (PTX), a chemotherapeutic drug frequently used in cancer treatment, at the gene and protein levels. To this end, 6 groups were formed: control, PTX, sham, 1 mg/PTL, 2 mg/kg PTL, and 4 mg/kg PTL. Pain formation was tested by Randall-Selitto analgesiometry and locomotor activity behavioral analysis. Then, PTL treatment was performed for 14 days. After the last dose of PTL was taken, Hcn2, Trpa1, Scn9a, and Kcns1 gene expressions were measured in rat brain (cerebral cortex/CTX) tissues. In addition, changes in the levels of SCN9A and KCNS1 proteins were determined by immunohistochemical analysis. Histopathological hematoxylin-eosin staining was also performed to investigate the effect of PTL in treating tissue damage on neuropathic pain caused by PTX treatment. When the obtained data were analyzed, pain threshold and locomotor activity decreased in PTX and sham groups and increased with PTL treatment. In addition, it was observed that the expression of the Hcn2, Trpa1, and Scn9a genes decreased while the Kcns1 gene expression increased. When protein levels were examined, it was determined that SCN9A protein expression decreased and the KCNS1 protein level increased. It was determined that PTL treatment also improved PTX-induced tissue damage. The results of this study demonstrate that non-opioid PTL is an effective therapeutic agent in the treatment of chemotherapy-induced neuropathic pain, especially when used at a dose of 4 mg/kg acting on sodium and potassium channels.

The chemotherapeutic agent paclitaxel (PTX) causes testicular toxicity due to oxidative stress. Parthenolide (PTL), the active ingredient of the Tanacetum parthenium plant, is used to treat inflammation, dizziness, and spasms. In the present study, we evaluated the therapeutic effect of PTL on PTX-induced testicular toxicity in rats and its role in reproductive function. To this end, 6 groups were formed: control, PTX, sham, T1, T2, and T3. After testicular toxicity was induced in rats with 8 mg/kg PTX, the rats were treated with 1 mg/kg, 2 mg/kg, and 4 mg/kg PTL for 14 days. GSH and MDA levels were measured in rat testicular tissue after the last dose of PTL was administered. To determine the damage caused by PTX to testicular tissue by detecting 8-OHdG and iNOS, sections were prepared and examined histopathologically and immunohistochemically. Furthermore, the gene expressions and enzymatic activities of SOD, CAT, GPx, GST, and GR were investigated in all groups. After PTL treatment, MDA, 8-OHdG, and iNOS levels decreased while GSH levels increased in testicular tissue. Increased levels of antioxidant genes and enzymes also reduced oxidative stress. Additionally, the expression levels of the Dazl, Ddx4, and Amh genes, which are involved in gametogenesis and sperm production, decreased in case of toxicity and increased with PTL treatment. The data from this study show that PTL may have a therapeutic effect in the treatment of testicular damage by eliminating the oxidative stress-induced damage caused by PTX in testicular tissue, providing an effective approach to alleviating testicular toxicity, and playing an important role in reproduction/sperm production, especially at a dose of 4 mg/kg.