Effect of taxifolin on acrylamide-induced oxidative and proinflammatory lung injury in rats: Biochemical and histopathological studies

Purpose: To examine the probable beneficial effects of taxifolin against acrylamide damage in lung tissue.Methods: 18 male albino Wistar rats were divided into healthy (HG), acrylamide (AG) and taxifolin + acrylamide (TAG) groups. Once a day for 30 days, acrylamide was orally administered to the AG group (50 mg/kg), while ACL (50 mg/kg) and TAX (20 mg/kg) were orally administered to TAG group. Protein concentration, malondialdehyde (MDA), and total glutathione (tGSH) levels as well as oxidant and antioxidant molecules concentrations of the rat lung tissues were measured. In addition, degree of mononuclear (MN) cell infiltration and bronchial-associated lymphoid tissue (BALT) hyperplasia was evaluated by the degree of hyperplasia (absent, mild, moderate, severe). The histopathological andbiochemical data the groups were compared.Results: When compared in terms of MDA levels, it was found that the AG group had high MDA levels, and the TAG group had low MDA levels. (p < 0.001). TAG group was found to have a higher tGSH level than the AG group (p < 0.001). Compared to the AG group, lower TOS and higher TAS levels were obtained in the TAG group (p < 0.001). In addition, when TOS levels of TAG and HG groups were compared, the TOS levels between the two groups were statistically insignificant (p = 0.213). It has been observed that TAX administration prevents the increase in NF-ƘB level. When the NF-ƘB levels of the AG and TAG groups were compared with each other, there was a statistically significant difference (p = 0.001). In the AG group, severe MN cell hyperplasia and BALT hyperplasia were observed histopathologically. It was determined that these findings were alleviated in the TAG group. A histopathologically significant difference was found between AG and TAG groups (p < 0.05).Conclusion: Taxifolin has beneficial effects against lung injury caused by acrylamide, a healthdamaging environmental factor. Regular use of taxifolin can be recommended, especially in people who are known to have intense contact with acrylamide. There is a need for research studies on this subject

Effect of taxifolin on methotrexate-induced oxidative and inflammatory oral mucositis in rats: biochemical and histopathological evaluation

The role of oxidative stress, as well as inflammation in the pathogenesis of methotrexate (MTX)-induced oral mucositis, is a known fact. The anti-inflammatory, antitumor, antimicrobial, and antioxidant properties of taxifolin—the effect we tested against MTX-induced oral mucosal damage—are well known. Objective: Evaluating biochemically and histopathologically the effects of taxifolin on methotrexate-induced oral mucosal damage in rats. Methodology: In the taxifolin+MTX (TMTX) group, 50 mg/kg taxifolin was orally administered to rats by gavage. In the MTX and healthy (HG) groups, normal saline was applied to rats as solvent by the same method. One hour after administration of taxifolin and solvent, 5 mg/kg MTX was orally administered to rats in the MTX and TMTX groups. Taxifolin and methotrexate were administered once a day for 30 days. Macroscopic, biochemical, and histopathological evaluations were performed on the inner cheek and tongue tissues of rats. These parts were removed after rats were killed with a high-dose anesthesia. Results: Taxifolin with MTX prevented the increase in oxidant and pro-inflammatory parameters, such as malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), on the inner cheek and tongue tissues of rats. Moreover, taxifolin antagonized the decrease in total glutathione (tGSH). Taxifolin decreased MTX-induced histopathological damage. Conclusion: These findings suggest that taxifolin may be useful to treat MTX-associated oral mucositis

Protective effect of cinnamon extract against cobalt-induced multiple organ damage in rats

BackgroundThe role of oxidative stress and inflammation in cobalt (Co) toxicity has been the focus of previous studies. Cinnamon and its main components have been reported to have protective effects in various tissues with antioxidant and anti-inflammatory effects.AimsIn this study, the protective effect of cinnamon extract (CE) against possible Co-induced heart, kidney, and liver damage in rats was investigated biochemically.MethodsEighteen albino Wistar-type male rats were categorized into three groups (n = 6 per group): control (CG), CoCL2-administered (CoCL2), and CE + CoCL2-administered (CE + Co) groups. The CE + CoCL2 group was administered CE (100 mg/kg), and the CoCL2 and CG groups were administered distilled water orally by gavage. One hour after the administration, Co (150 mg/kg) was administered orally to the CE + CoCL2 and CoCL2 groups. This procedure was repeated once daily for 7 days. Then, biochemical markers were studied in the excised heart, kidney, and liver tissues.ResultsCoCL2 increased oxidants and proinflammatory cytokines and decreased antioxidants in heart, kidney, and liver tissues. Heart, kidney, and liver tissue were affected by Co damage. CE treatment suppressed the CoCL2-induced increase in oxidants and proinflammatory cytokines and decrease in antioxidants in heart, kidney, and liver tissues. CE treatment has been shown to attenuate cardiac damage by reducing serum troponin I (TpI) and creatine kinase-MB (CK-MB), renal damage by reducing creatinine and blood urea nitrogen (BUN), and liver damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST).ConclusionCo induced the production of oxidants and proinflammatory parameters and antioxidant depletion in heart, kidney, and liver tissues of rats. Our experimental results show that CE protects heart, kidney, and liver tissues against oxidative and inflammatory changes induced by CoCLl2

Lacidipine, thiamine pyrophosphate and their combination on the ocular ischemic syndrome induced by bilateral common carotid artery ligation

AIM: To investigate the effect of lacidipine, thiamine pyrophosphate (TPP) and the combination of lacidipine and TPP against oxidative and inflammatory eye damage induced by bilateral common carotid artery ligation in rats. METHODS: Male albino Wistar rats were categorized as those who underwent sham surgery (SG), right and left common carotid cross-clamping and unclamping procedure (CCU), lacidipine+CCU (LCCU), TPP+CCU (TCCU), and combination of lacidipine and TPP (LTC)+CCU (LTCCU). One hour before anesthesia, the LCCU (n=6) received lacidipine (4 mg/kg, orally) and the TCCU (n=6) received TPP (20 mg/kg, intraperitoneally). The SG (n=6) and CCU (n=6) received the same volume of distilled water from the same route. After anesthesia (60 mg/kg ketamine, intraperitoneally), the necks of the rats were opened in the midline. Ischemia was created for 10min by placing clips on the right and left common carotid arteries. Rats in the SG only underwent subcutaneous incision. After 10min, the clips were removed and reperfusion was achieved for six days. Then, the animals were euthanized (120 mg/kg ketamine, intraperitoneally) and the levels of oxidant, antioxidant and proinflammatory cytokines in the eye tissues were determined. The retinal tissue of the eye was also examined histopathologically. RESULTS: Lacidipine, TPP, and LTC significantly prevent the increase in malondialdehyde, tumor necrosis factor-alpha, interleukin-1β (IL-1β), and IL-6 levels, decrease in total glutathione levels, superoxide dismutase and catalase activities and histopathological retinal damage in eye tissue induced by bilateral common carotid artery ligation in rats. The impact of these drugs on protection is determined to be LTC>lacidipine>TPP. CONCLUSION: As a result of the study, it is concluded that LTC may be more effective than lacidipine and TPP alone in treating ocular ischemic syndrome

The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats

Abstract Acrylamide is a neurotoxic compound. Moreover, anakinra is an interleukin-1 (IL-1) receptor antagonist used in rheumatoid arthritis treatment. This study investigated the effect of anakinra on acrylamide-related neuropathy and neuropathic pain. Acrylamide exposure caused a significant decrease in the pain threshold; an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) levels; and a decrease in total glutathione (tGSH) values in the sciatic nerve. This indicates hyperalgesia presence, oxidative stress, and peripheral nerve tissue inflammation. Anakinra treatment significantly reduced the MDA, IL-1β, and TNF-α levels, and increased the pain threshold and mean tGSH values. The analgesic effect of anakinra was 67.9% at the first hour, increasing to 74.9% and 76.7% at the second and third hours, respectively. The group receiving acrylamide exhibited histopathological changes (e.g., swollen and degenerated axons, hypertrophic and hyperplasic Schwann cells, and congested vessels). The use of anakinra significantly improved these morphological changes. Anakinra is concluded to reduce neuropathic pain and prevent neurotoxic effect of acrylamide on peripheral nerves due to its analgesic, antioxidant, and anti-inflammatory properties

Protective effect of nimesulide on the external ear damage induced by staphylococcus aureus inoculation in rats

Since the external ear is covered with skin, infections that cause otitis externa are often produced by distinct skin flora in several different areas. Staphylococcus aureus (S. aureus) reproduces the most out of all bacteria isolated from external auditory canal skin culture samples. Proinflammatory cytokines are the main components responsible for tissue damage pathogenesis due to S. aureus. Nimesulide is a nonsteroidal anti-inflammatory drug that selectively inhibits cyclooxygenase-2 and also demonstrates antioxidant properties. The present study aimed to examine the antibacterial activity of nimesulide against S. aureus and to compare its effectiveness on otitis externa induced by S. aureus in male albino Wistar rats with that of cefazolin. The antimicrobial activity testing was conducted using the Kirby-Bauer disk diffusion method as described by the European Committee on Antimicrobial Susceptibility Testing. To induce otitis externa, we applied 0.5 ml of S. aureus to the ear skin using a hypodermic syringe (S. aureus strain TACK 25923 was dispersed on the 900x10-6 concentration of colony forming units per ml). Nimesulide and cefazolin were administered orally at a dose of 50 mg/kg. The antibacterial activity of cefazolin when used in equal doses (50 µg/ml) was more powerful against S. aureus than nimesulide. However, nimesulide reduced the macroscopic findings (such as oedema and redness) induced by S. aureus better than cefazolin. Additionally, nimesulide inhibited the increase of oxidant and proinflammatory indicators related to S. aureus, while cefazolin was able to inhibit only the increase in proinflammatory indicators. Our results showed that nimesulide was superior to cefazolin in terms of reducing the external ear damage caused by S. aureus. Therefore, nimesulide monotherapy or a combination of nimesulide and cefazolin therapy may be beneficial in the treatment of bacterial otitis externa. [Med-Science 2021; 10(2.000): 577-82

Protective effect of lutein against acrolein-induced ototoxicity in rats

Background: Acrolein is a reactive aldehyde that forms during burning of wood and other fuels. It is also a product of lipid peroxidation (LPO) reactions and is present in cigarette smoke. Acrolein is known to cause oxidative stress and inflammatory nerve tissue damage. Lutein is a tetraterpenoid molecule with antioxidant and anti-inflammatory properties. There appear to be no studies on the effect of lutein on vestibulocochlear nerve damage induced by acrolein. The aim of this study was to investigate the effect of lutein on vestibulocochlear nerve damage induced by acrolein in rats using biochemical and histopathological methods. Methods: The rats were divided into three groups (n = 6, for each group) a healthy control group (HG), an acrolein (ACR) group and a lutein and acrolein (LACR) group. In the LACR group, lutein was administered (1 mg/kg) via oral gavage. The ACR and HG groups received saline via oral gavage. Then, 1 h after the administration of lutein and saline, the LACR and ACR groups were treated with 3 mg/kg of acrolein via oral gavage. This procedure was repeated once a day for 30 days. Results: The results of biochemical experiments showed that in the vestibulocochlear nerve tissues of the animals treated with acrolein, the levels of malondialdehyde, total oxidants, nuclear factor kappa b, tumor necrosis factor alpha and interleukin 1 beta significantly increased, whereas the levels of total glutathione and total antioxidants decreased as compared to those in the HG and LACR groups. In addition, severe histopathological damage was observed in vestibulocochlear nerve tissue of the acrolein group, whereas this damage was alleviated in the lutein group. Conclusion: Lutein protected vestibulocochlear nerve tissue from acrolein-associated oxidative and proinflammatory damage. This suggests that lutein might be useful in preventing or treating acrolein-induced ototoxicity

Effects of nimesulide on the small intestine mucositis induced by methotrexate in rats

Intestinal mucositis is one of the major problems in the patients receiving cancer treatment. Nimesulide is a drug with antioxidant, antiinflammatory and antiulcer features. We aimed to investigate the effect of nimesulide on the small intestine mucositis induced by methotrexate (MTX) in rats. Experimental animals were divided into the control group, MTX group (MTXG) and nimesulide+MTX administered group (NMTXG) with eight rats per group. The control and MTXG groups were given distilled water by gavage and the NMTXG was given nimesulide 100 mg/kg orally. After one hour, the NMTXG and MTXG rat groups were administered oral MTX 5 mg/kg. This procedure was repeated once a day for 15 days and the rats were sacrificed. The duodenum and jejunum of each rat was removed for the assessment of biochemical markers and histopathological evaluation. Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were significantly higher in the duodenal and jejunal tissues of the animals which received MTX, compared to the control and NMTXG (P<0.001). Also, the levels of total glutathione (tGSH), glutathione reductase (GSHRd), glutathione peroxidase (GSHPx), catalase (CAT) and superoxide dismutase (SOD) were significantly lower in the MTXG (P<0.001) compared to other groups. MTX led to villus and crypt epithelial damage and inflammation containing marked PMNL and eosinophils in the intestinal tissues histopathologically. Whereas, there was only mild irregularities in the villus structures of the NMTXG. Nimesulide protected the small intestines against damage by MTX. Intestinal mucositis caused by MTX may be preventable by co-administered nimesulide