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Mercuric chloride (HgCl2) is extremely toxic to both humans and animals. It could be absorbed via ingestion, inhalation, and skin contact. Exposure to HgCl2 can cause severe health effects, including damages to the gastrointestinal, respiratory, and central nervous systems. The purpose of this work was to explore if carvacrol (CRV) could protect rats lungs from damage caused by HgCl2. Intraperitoneal injections of HgCl2 at a dose of 1.23 mg/kg body weight were given either alone or in conjunction with oral CRV administration at doses of 25 and 50 mg/kg body weight for 7 days. The study included biochemical and histological techniques to examine the lung tissue's oxidative stress, apoptosis, inflammation, and autophagy processes. HgCl2‐induced reductions in GSH levels and antioxidant enzymes (SOD, CAT, and GPx) activity were enhanced by CRV co‐administration. Furthermore, MDA levels were lowered by CRV. The inflammatory mediators NF‐κB, IκB, NLRP3, TNF‐α, IL‐1β, IL6, COX‐2, and iNOS were all reduced by CRV. When exposed to HgCl2, the levels of apoptotic Bax, caspase‐3, Apaf1, p53, caspase‐6, and caspase‐9 increased, but the levels of antiapoptotic Bcl‐2 reduced after CRV treatment. CRV decreased levels of Beclin‐1, LC3A, and LC3B, which in turn decreased HgCl2‐induced autophagy damage. After HgCl2 treatment, higher pathological damage was observed in terms of alveolar septal thickening, congestion, edema, and inflammatory cell infiltration compared to the control group while CRV ameliorated these effects. Consequently, by preventing HgCl2‐induced increases in oxidative stress and the corresponding inflammation, autophagy, apoptosis, and disturbance of tissue integrity in lung tissues, CRV might be seen as a useful therapeutic alternative. [ABSTRACT FROM AUTHOR]

Objective(s): The present study investigated whether morin has a protective effect against ACRinduced cardiac toxicity. Materials and Methods: In this study, oxidative stress, inflammation, endoplasmic reticulum stress (ERS), and apoptosis markers in heart tissues were analyzed by different methods after ACR (38.27 mg/kg) and morin (50 or 100 mg/kg) oral administration for ten days to Sprague Dawley rats. Results: The data obtained showed that ACR induced lipid peroxidation by decreasing superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) enzyme activities, glutathione (GSH) levels and nuclear factor erythroid 2-related factor 2 (Nrf-2), heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase quinone 1 (NQO1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC) gene expressions. On the other hand, these markers approached the control group levels after morin treatment. Moreover, morin suppressed ACR-induced inflammatory genes. Morin down-regulated the related genes by reducing the ERS, exacerbated after ACR administration. In addition, it was observed that B-cell lymphoma-2 (Bcl-2) associated X protein (Bax), caspase-3, and apoptotic peptidase activating factor 1 (apaf-1) expressions, elevated by ACR in the heart tissue, were suppressed after morin administration. Moreover, Bcl-2 expression was triggered by morin treatment. Thus, morin suppressed ACR-induced apoptosis. Conclusion: Taken together, morin may protect against ACR-induced cardiac injury by suppressing oxidative stress, inflammation, ERS, and apoptosis. [ABSTRACT FROM AUTHOR]

Lead acetate (PbAc) is a compound that produces toxicity in many tissues after exposure. Sinapic acid (SNP) possesses many biological and pharmacological properties. This study aimed to investigate the efficacy of SNP on the toxicity of PbAc in lung tissue. PbAc was administered orally at 30 mg/kg and SNP at 5 or 10 mg/kg for 7 days. Biochemical, genetic, and histological methods were used to investigate inflammatory, apoptotic, endoplasmic reticulum stress, and oxidative stress damage levels in lung tissue. SNP administration induced PbAc‐reduced antioxidant (GSH, SOD, CAT, and GPx) and expression of HO‐1 in lung tissue. It also reduced MDA, induced by PbAc, and thus alleviated oxidative stress. SNP decreased the inflammatory markers NF‐κB, TNF‐α and IL‐1β levels induced by PbAc in lung tissue and exhibited anti‐inflammatory effect. PbAc increased apoptotic Bax, Apaf‐1, and Caspase‐3 mRNA transcription levels and decreased anti‐apoptotic Bcl‐2 in lung tissues. SNP decreased apoptotic damage by reversing this situation. On the other hand, SNP regulated these markers and brought them closer to the levels of the control group. PbAc caused prolonged ER stress by increasing the levels of ATF6, PERK, IRE1α, GRP78 and this activity was stopped and tended to retreat with SNP. After evaluating all the data, While PbAc caused toxic damage in lung tissue, SNP showed a protective effect by reducing this damage. [ABSTRACT FROM AUTHOR]

Objective(s): This study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA). Materials and Methods: In the study, five groups were formed (n=7) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG 25 group, and SA+ZNG 50 group. While SA was administered orally to rats at 10 mg/kg/bw, ZNG was given to rats orally at 25 and 50 mg/kg/bw doses for 14 days. Results: As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-κB, TNF-α, IL-1β, and IL-6 were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP3, and JAK-2/STAT3 gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-6, PERK, IRE1, and GRP78 genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-3 expressions and inhibiting Bcl-2 expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality. Conclusion: ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles. [ABSTRACT FROM AUTHOR]

Objective(s): In the present study, the potential protective effects of zingerone (ZNG) against sciatic nerve damage caused by sodium arsenite (SA), a common environmental pollutant, were evaluated by various biochemical, molecular, and histological methods. Materials and Methods: In the study, SA and ZNG were given to 35 male Sprague Dawley rats for 14 days. At the end of the period, the sciatic nerve tissues were taken and the markers involved in oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis were analyzed. Results: The data obtained showed that SA decreased glutathione (GSH) levels and increased malondialdehyde (MDA) levels in the sciatic nerve tissue. However, it was determined that these markers approached the control group levels due to the anti-oxidant properties of ZNG. While SA triggered endoplasmic reticulum stress and apoptosis pathways, ZNG suppressed them. Moreover, SA up-regulated inflammatory markers such as nuclear factor kappa-B (NF-κB), tumor necrosis factoralpha (TNF-α), interleukin-1-beta (IL-1β), and neuronal nitric oxide synthases (nNOS) in the sciatic nerves and caused neuro-inflammation and inhibited cell survival by suppressing serine/threonineprotein kinase 2 (Akt2) and forkhead box protein O1 (FOXO1) genes. It has also been shown histopathologically that SA causes degeneration in the sciatic nerves. In contrast, ZNG suppressed neuro-inflammation, activated Akt2/FOXO1 signaling, and repaired histological irregularities. Conclusion: In general, SA caused oxidative stress, inflammation, ER stress, and apoptosis in the sciatic nerves of rats, causing damage to the tissues, however, ZNG suppressed these pathways and protected the sciatic nerves from the destructive effect of SA. [ABSTRACT FROM AUTHOR]

Objective(s): In the present study, it was evaluated whether morin has a protective effect on testicular toxicity caused by ifosfamide (IFOS), which is used in the treatment of various malignancies. Materials and Methods: For this purpose, 100 or 200 mg/kg morin was given to Sprague Dawley rats for 2 days, and a single dose (500 mg/kg) IFOS was administered on the 2nd day. At the 24th hr of IFOS administration, animals were decapitated and testicular tissues were taken and the status of oxidative stress, inflammation, endoplasmic reticulum stress (ERS), autophagy, and apoptosis markers were analyzed by biochemical, molecular, and histopathological methods. Results: According to the data obtained, it was determined that IFOS caused oxidative stress in testicular tissues. It was observed that inflammation, ERS, autophagy, apoptosis, and oxidative DNA damage occurred with oxidative stress. Morin treatment suppressed oxidative stress. Morin showed anti-inflammatory effects by reducing TNF-α and IL-1β protein levels. It also increased the mRNA transcript levels of the ERS marker ATF-6, PERK, IRE1, GRP-78, and CHOP genes, and the apoptosis marker genes Bax, Casp-3, and apaf-1. It up-regulated the anti-apoptotic protein Bcl-2 gene and the cell survival signal AKT-2 gene. Morin caused a decrease in beclin-1 protein levels and showed an anti-autophagic effect. In addition, morin attenuated oxidative DNA damage and decreased 8-OHdG immune-positive cell numbers. Conclusion: As a result, it was observed that IFOS caused cellular damage by activating various signaling pathways in testicular tissue, while morin exhibited protective properties against this damage. [ABSTRACT FROM AUTHOR]

Background: Scabies is one of the most common diseases in dogs. It threatens both animals and humans due to its zoonotic potential. Objective: The purpose of this study was to evaluate the oxidant/antioxidant balance with hematological findings in dogs infested with sarcoptic mange. Methods: The animals evaluated in this study consisted of 32 mixed-breed dogs between 1 and 2 years of age. The dogs were allocated into two groups: a control group (infestation-free animals; n=10), and a sarcoptic mange-infected group (Sarcoptes, n=22). Dogs in the Sarcoptes group showed infestation signs such as intense itching, excoriations, alopecia, and blistering of the elbow and auricular margins. Results: Significant increase (p<0.01) levels were observed in total oxidant status (TOS), malondialdehyde (MDA), oxidative stress index (OSI), and nitric oxide (NO), while glutathione (GSH) and total antioxidant status (TAS) levels in dogs infested with Sarcoptes decreased significantly (p<0.01). In addition, a significant increase (p<0.01) of WBC count in dogs in the sarcoptic group in comparison with the control was found. Conversely, there was significant decrease (p<0.01) in RBC, HGB, and PCV counts in Sarcoptes-infested dogs. Conclusions: Our study suggests a possible relationship between oxidant/antioxidant imbalance and hematological findings in dogs infested with sarcoptic mange. Furthermore, in addition to MDA, TAS, TOS, and OSI markers, NO as well as GSH might be also used to assess the oxidative stress in dogs naturally infected with Sarcoptes scabiei. [ABSTRACT FROM AUTHOR]

In this study, we aimed to investigate haematological, pro‐inflammatory, inflammatory, anti‐inflammatory and immunological responses in naturally Theileria annulata‐infected cattle. The study material consisted of 25 Simmental cattle, 2–4 years of age, one of which was a control group consisting of healthy animals (Control group, n = 10), and the other was a Theileria group that include animals positive for Theileria annulata (Theileria group, n = 15). Haematological analysis (red blood cell [RBC], haemoglobin [HGB], haematocrit [HCT]), pro‐inflammatory (tumour necrosis factor‐α [TNF‐α], nuclear factor kappa B [NF‐ĸB] and interleukin‐1 beta, [IL‐1β]), inflammatory (neutrophil‐lymphocyte ratio [NLR]), anti‐inflammatory (interleukin‐10 [IL‐10]) and antimicrobial peptide (CAMP) analyses were performed by using ELISA kit from blood samples. It was found that the rectal temperature of the Theileria group was found to be significantly higher (p <.001) than that of the control group. Haematological and biochemical analysis revealed that the RBC and HGB count and HCT percentage decreased (p <.001), while NF‐ĸB (p <.001), TNF‐α (p =.002), IL‐1β (p <.001), IL‐10 (p =.012), NLR (p <.001) and CAMP (p =.037) levels increased in Theileria group compared to the control group. There was a strong correlation between NF‐ĸB and TNF‐α, NF‐ĸB and IL‐10, NLR and IL‐1β, NF‐ĸB and CAMP, TNF‐α and CAMP and IL‐10 and CAMP. As a result of this study, it was revealed that a pro‐inflammatory and immunological response also occurs along with the anti‐inflammatory response in the inflammatory process. [ABSTRACT FROM AUTHOR]

In this study, the effects of Aloe vera gel and coconut oil on wound healing were investigated and compared in rats. Forty-two Wistar albino rats were used during the experiment, in which they were operated on under general anaesthesia to create two full-thickness open skin wounds (created with a 0.5 cm diameter punch biopsy apparatus) on both back sides of the median line. A total of 42 rats were divided into three groups of 14 animals each to receive the topical application of Aloe vera gel (AV group – n = 14), coconut oil (CO group – n = 14) and cold cream (CONT group – n = 14). The medical applications were performed twice a day in all the groups. The wound borders were marked on a transparent sheet every day. Afterwards, this sheet was transferred to the millimetre graph paper. On days 0, 7, and 14, the unhealed wound area was measured in all the groups. On days 7 and 14, seven rats in each group were euthanised. Then, skin samples including the intact skin were taken from the wound sites for histopathological and biochemical evaluations. The topical application of Aloe vera gel showed a significant increase in the healing process of the open wounds in terms of the clinical evaluation, histopathological and biochemical data averages when compared with the coconut oil and cold cream groups of rats (P < 0.05). The results obtained in the present study demonstrate that Aloe vera gel may provide a good alternative for the treatment of open wounds. [ABSTRACT FROM AUTHOR]

Morin is a flavonoid and broadly found in white berry and cranberry branch. Ifosfamide (IFOS) is known as an anticancer and cytotoxic drug especially on the liver. This study aimed to explore the potential protective effects of Morin against IFOS-induced liver toxicity in rats. The model group of rats received a single injection of IFOS (500 mg/kg; i.p.) at day 2, whereas the protective groups of rats were given two different doses of Morin (100 and 200 mg/kg; given by gavage) at days 1 and 2. All animals were then culled 24 h post-IFOS injection. We observed that IFOS caused liver injury, oxidative stress, inflammation, DNA damage, and apoptosis. However, Morin decreased the levels of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT) (p < 0.05). While Morin contributed to the recovery of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH) levels, Morin decreased the levels of malondialdehyde (MDA) induced by IFOS in the liver (p < 0.05). Besides, the levels of nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), and P53 measured by ELISA test were reduced via Morin administration (p < 0.05). Lastly, the mRNA transcript levels of Bax, Apaf-1, Bcl-2, Bcl-xL, and inducible nitric oxide synthase (iNOS) determined by RT-PCR were down-regulated in the Morin groups (p < 0.05). These results indicate that Morin plays a protective role by reducing oxidative stress, inflammation, and apoptosis in the IFOS-induced liver injury in rats. [ABSTRACT FROM AUTHOR]

This study investigated the effects of rutin against reproductive damage caused by toxic mercury in male rats. Thirty‐five Sprague Dawley rats were used. Control group was injected with saline for 7 days. The rutin‐100 group received 100 mg/kg/b.w. rutin for 7 days. Mercuric chloride (HgCl2) group received 1.23 mg/kg/b.w. of HgCl2 for 7 days. Mercury chloride + rutin‐50 group received 50 mg/kg/b.w. rutin and HgCl2 1.23 mg/kg/b.w. for 7 days. HgCl2 + rutin‐100 group received 100 mg/kg/b.w. rutin and HgCl2 1.23 mg/kg/b.w. for 7 days. It was detected that HgCl2 treatment increased malondialdehyde (MDA) levels, tumour necrosis factor‐α (TNF‐α) and cyclooxygenase‐2 (COX‐2) expressions, necrosis and degeneration of spermatogonium, dead and abnormal sperm percentages; tubular walls thinning; and decreased antioxidant enzyme activities and sperm motility. It was determined that rutin application reduced testicular damage caused by HgCl2. In conclusion, rutin administration may treat HgCl2 toxicity in testes. [ABSTRACT FROM AUTHOR]

Doxorubicin (DXR) is one of the most important chemotherapeutic agent. However, nephrotoxicity reduces its clinical utility in humans. The aim of the study was to investigate protective effects of curcumin (CMN) against DXR-induced nephrotoxicity. Rats were subjected to oral treatment of CMN (100 and 200 mg/kg body weight) for 7 days. Nephrotoxicity was induced by single intra peritoneal injection of DXR (40 mg/kg body weight) on the fifth day and then the experiment was terminated on the eighth day. Nephroprotective effects of CMN were associated with decrease in serum toxicity markers and increase in antioxidant enzyme activities. CMN was able to reduced the levels of inflammatory markers such as TNF-α, NF-κB, IL-1β, iNOS and COX-2 in the rats. It also reduced the expressions of apoptotic marker including caspase-3, and oxidative DNA damage marker including 8-OHdG. Collectively, these findings indicated that CMN protect against DXR-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

Abstract: Doxorubicin (DXR) is a highly effective drug for chemotherapy. However, cardiotoxicity reduces its clinical utility in humans. The present study aimed to assess the ameliorative effect of curcumin against DXR‐induced cardiotoxicity in rats. Rats were subjected to oral treatment of curcumin (100 and 200 mg/kg body weight) for 7 days. Cardiotoxicity was induced by single intraperitoneal injection of DXR (40 mg/kg body weight) on the 5th day and the rats sacrificed on 8th day. Curcumin ameliorated DXR‐induced lipid peroxidation, glutathione depletion, decrease in antioxidant (superoxide dismutase, catalase, and glutathione peroxidase) enzyme activities, and cardiac toxicity markers (CK‐MB, LDH, and cTn‐I). Curcumin also attenuated activities of Caspase‐3, cyclooxygenase‐2, inducible nitric oxide synthase, and levels of nuclear factor kappa‐B, tumor necrosis factor‐α, and interleukin‐1β, and cardiac tissue damages that were induced by DXR. Moreover, curcumin decreased the expression of 8‐OHdG and 3,3′‐dityrosine. This study demonstrated that curcumin has a multi‐cardioprotective effect due to its antioxidant, anti‐inflammatory, and antiapoptotic properties. [ABSTRACT FROM AUTHOR]

Paracetamol (PC) is a widely used analgesic and antipyretic drug, but it leads to acute hepatotoxicity at high doses intakes. This study was aimed to investigate the effects of Chrysin (CR) on hepatotoxicity constituted at high doses of PC in rats. Rats were subjected to oral pretreatment of CR (25 and 50 mg/kg b.w.) via feeding needle for 6 days against hepatotoxicity induced by a single dose of PC (500 mg/kg b.w.) administered orally via feeding needles. Although PC increases lipid peroxidation and liver enzyme activities, it has led to reduction of antioxidant enzyme activities. PC induced inflammatory responses by increasing the levels of TNF-α and IL-1β. Furthermore, PC caused apoptosis and autophagy by increasing activity of Caspase-3 and LC3B level. On the other hand, CR therapy significantly regulated these values in rats. This study demonstrated that CR possesses restorative effect against PC-induced hepatotoxicity by suppressing oxidative stress, inflammation, and apoptotic and autophagic tissue damage. [ABSTRACT FROM AUTHOR]

Silymarin (SLY) and naringin (NRG) are natural flavonoids that have been reported to have many benefits and medicinal properties. The present study was designed to investigate the protective effect of SLY and NRG against methotrexate (MTX)-induced nephrotoxicity in experimental animals. Rats were subjected to oral pretreatment of SLY (25 and 50 mg/kg body weight (b.w.)/day) and NRG (50 and 100 mg/kg b.w./day) for 7 days against renal toxicity induced by single intraperitoneal administration of MTX (20 mg/kg b.w.). MTX resulted in an increase in serum toxicity markers, lipid peroxidation, and reduction in activities of antioxidant enzymes. Additionally, MTX provoked inflammatory responses by increasing the levels of TNF-α, IL-1β, IL-6, NF-κB, and activation of COX-2 and iNOS. Furthermore, MTX administration caused apoptosis and autophagy by increasing activity of Caspase-3 and light chain 3B level. Conversely, SLY and NRG therapy significantly decreased these values in rats. This study demonstrated that SLY and NRG protect against MTX-induced nephrotoxicity. Practical applications Chemotherapeutic drugs have been used for cancer treatment for many years. However, in the treatment process, they may damage organs such as liver and kidney, prolong the treatment process and negatively affects patient welfare. This study revealed that silymarin and naringin exhibited potent anti-inflammatory, antiapoptotic, and antiautophagic effect in renal injury caused by methotrexate, a chemotherapeutic drug. Therefore, treatment silymarin and naringin can be used for the beneficial effect against methotrexate-induced kidney damage in cancer chemotherapy. [ABSTRACT FROM AUTHOR]

Paracetamol (PC) is a safe analgesic and antipyretic drug at therapeutic doses, and it is widely used in clinics. However, at high doses, it can induce hepatotoxicity and nephrotoxicity. Chrysin (CR) is a natural flavonoid that has biological activities that include being an antioxidant, an anti-inflammatory, and an anti-cancer agent. The main objective of this study was to investigate the efficacy of CR against PC-induced nephrotoxicity in rats. CR was given orally via feeding needle to male Sprague Dawley rats as a single daily dose of 25 or 50 mg/kg for six days. PC was administered orally via feeding needle as a single dose on the sixth day. PC caused significant glutathione depletion, lipid peroxidation, increased serum toxicity markers (serum urea and creatinine), and reductions in activities of antioxidant enzymes (superoxide dismutase -- SOD, catalase -- CAT, and glutathione peroxidase -- GPx). The renal protective effect of CR was associated with decreasing the regulation of serum renal toxicity markers and increasing the regulation of antioxidant enzyme activities. Additionally, PC led to significant increases in the levels of inflammatory markers including tumour necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-33 (IL-33). Furthermore, PC induced apoptotic tissue damage by increasing cysteine aspartate-specific protease-3 (caspase-3) activity and autophagic tissue damage by increasing the expression of light chain 3B (LC3B). CR therapy significantly decreased these values in rats. This study demonstrated that CR has antioxidant, anti-apoptotic, anti-inflammatory and anti-autophagic effects on PC-induced kidney toxicity in rats. [ABSTRACT FROM AUTHOR]

Introduction: Patients with diabetic kidney disease (DKD) are more prone to contrast-induced nephropathy (CN). Apoptosis and autophagy were found to be essential in the pathogenesis of DKD. Interleukin-33 (IL-33) is a cytokine, but its role in DKD and CN is unknown. As IL-33 is modulated by apoptosis, we aimed to determine the relationship between IL-33 apoptosis and autophagy in DKD with CN.Materials and methods: Thirty male Sprague–Dawley rats were enrolled and randomly allocated into three groups. The first group was comprised of healthy rats (HRs), whereas the other two groups were made up of diabetic rats (DRs) and diabetic rats with CN (DRs + CN). All groups except the HRs received 50 mg/kg/day of streptozotocin (STZ). The DRs + CN group was induced by administering 1.5 mg/kg of intravenous radiocontrast dye on the 35th day.Results: We observed increased IL-33 in the kidney tissue following induction of CN in the DRs. The DRs showed moderate immunopositivity, and the DRs + CN showed severe immunopositivity for caspase-3, cleaved caspase-3, caspase-8, caspase-9, LC3B, and Beclin-1 in tubular cells and glomeruli. The DRs also showed moderate immunopositivity in tubular cells, and the DRs + CN group showed severe immunopositivity for IL-33 in tubular cells. Increased caspase-3 was found in both glomeruli and tubuli; however, we could not demonstrate IL-33 in glomeruli. This could be secondary to inactivation of IL-33 via increased caspase-3 activity.Conclusion: The release of IL-33 from necrotic cells might induce autophagy, which can further balance the effects of increased apoptosis secondary to CN in DKD. [ABSTRACT FROM PUBLISHER]

• Silymarin protects against the brain and sciatic nerve injuries induced by docetaxel. • Silymarin activates Nrf2/HO-1, and suppresses Bax/Bcl2 signaling. • Docetaxel induces oxidative stress, inflammation and apoptosis. Docetaxel (DTX) is a chemotherapeutic agent used in the treatment of various malignancies but is often associated with central and peripheral neurotoxicity. The aim of this study was to investigate the neuroprotective effect of silymarin (SLM) against DTX-induced central and peripheral neurotoxicities in rats. Rats received 25 and 50 mg/kg body weight SLM orally for seven consecutive days after receiving a single injection of 30 mg/kg body weight DTX on the first day. SLM significantly decreased brain lipid peroxidation level and ameliorated brain glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in DTX-administered rats. SLM attenuated levels of nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), glial fibrillary acidic protein (GFAP) and activity of p38α mitogen-activated protein kinase (p38α MAPK) whereas caused an increase in levels of neural cell adhesion molecule (NCAM) in the brain and sciatic nerve of DTX-induced rats. In addition, SLM improved the histological structure of the brain and sciatic nerve tissues and decreased the expression of c-Jun N-terminal kinase (JNK) in the sciatic nerve whereas increased cyclic AMP response element binding protein (CREB) expression in the brain induced by DTX. Additionally, SLM markedly up-regulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and B-cell lymphoma-2 (Bcl-2) and downregulated the expression of Bcl-2 associated X protein (Bax) in the brain and sciatic nerve tissues of DTX-induced rats. Our results show that SLM can protect DTX-induced brain and sciatic nerve injuries by enhancing the antioxidant defense system and suppressing apoptosis and inflammation. [ABSTRACT FROM AUTHOR]

Testicular dysfunction or damage is among the critical side effects of chemotherapeutic drugs like cisplatin. This study was mapped out to assess the possible therapeutic effect of eugenol on cisplatin‐induced testicular damage. In this experimental study, a single dose of cisplatin (15 mg/kg) was given intraperitoneally. After 72 hr of cisplatin injection, rats were sacrificed and testis tissues were removed. Tissues were examined by biochemical, histopathological and immunohistochemical methods. While tissue lipid peroxidation product and apoptotic marker levels increased, antioxidant enzyme activities of testis tissue were decreased in the cisplatin group. Additionally, histopathological damage was also determined in testis tissue. Contrary to all these results, the severity of damage in the tissue was reduced histopathologically owing to eugenol treatment. The lipid peroxidation decreased and antioxidant enzyme activities increased in the eugenol treatment group. It has been determined that eugenol has a therapeutic effect on oxidative stress and apoptosis against cisplatin‐induced testicular damage. [ABSTRACT FROM AUTHOR]

In our work, it was purposed to investigate the effects of sodium arsenite (SA) and hesperidin (HSP) administered to rats on some metabolic enzymes including carbonic anhydrase (CA), aldose reductase (AR), paraoxonase‐1 (PON1), α‐glycosidase (α‐Gly), butyrylcholine esterase (BChE), acetylcholine esterase (AChE) enzymes activities in the brain, heart, liver, testis, and kidney tissues of rats. CA activities were significantly decreased in testis, liver, and heart tissues of rats given HSP, SA, SA+HSP‐100, and SA+HSP‐200 compared to control (p < 0.05). In liver tissue, AChE and BChE enzymes activities were significantly reduced given in all groups. In all tissues, α‐Gly activity was reduced given in all groups. In the current study, aldose reductase enzyme activity was reduced significantly in testis, brain, and heart tissues of all groups compared to standard (p < 0.05). PON1 enzyme activity was increased significantly in kidney and liver tissues of rats HSP groups and decreased SA groups compared to control. Practical applications: α‐Glycosidase is the key enzyme involved in the digestion of the carbohydrate. Another enzyme α‐amylase hydrolyzes the α‐linked polysaccharide derivatives into oligosaccharide molecules, and α‐glycosidase enzymes, which are characterized in small intestine, catalyze the final stage in the digestive mechanism of carbohydrate molecule to release absorbable monosaccharides like glucose. Conforming to the cholinergic hypothesis, impairment of the cholinergic pathways plays a good role in the development of neurodegenerative diseases like depression, schizophrenia, Alzheimer's disease (AD) problems with the regulation of traumatic brain injury and sleep. The AD is the main reason for dementia disease, and mild to moderate cases are generally treated with AChE inhibitors. Human CA inhibitor compounds are clinically used for more than 70 years as antiglaucoma and diuretics drugs. [ABSTRACT FROM AUTHOR]