ß-Glucan ameliorates cisplatin-induced oxidative and histological damage in kidney and liver of rats.

We investigated the effects of ß-glucan (ßg) on kidney and liver damage caused by cisplatin (CP), an antineoplastic agent widely used to treat many types of cancer, in a rat model. The side effects of CP in many tissues and organs limit its usage. ßg is a natural polysaccharide that is an effective free radical scavenger. A total of 28 rats were randomly divided into four groups. Group 1 was a non-intervention control, only feed and water were given. Group 2 was administered 7 mg/kg CP in a single dose. Group 3 was administered 50 mg/kg ßg orally for 14 days. Group 4 was administered ßg for 14 days, following a single dose of CP. At the end of the experiment, kidney and liver tissues were evaluated biochemically and histopathologically. Increased thiobarbituric acid-reactive substances (TBARS) levels, as well as decreased catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) levels, as well as histological damage, were noted in both the kidney and liver tissues of the CP group. However, ßg treatment prevented the oxidative and histopathological effects of CP. The study demonstrates the protective efficacy of ßg against CP-induced kidney and liver damage through the effect of its antioxidant properties.

Investigation of oxidative, inflammatory and apoptotic effects of favipiravir use alone and combined with vitamin C on brain tissue of elderly rats.

Favipiravir is a nucleoside analogue antiviral drug and inhibits the replication of many RNA viruses, especially influenza viruses. Favipiravir has also been used to treat patients with mild to moderate COVID-19 disease. However, various side effects, including neurological side effects, have been reported related to the use of favipiravir. Therefore, in this study, we aimed to investigate the possible effects of favipiravir alone or in combination with vitamin C on aged rats' brain tissue and the possible mechanisms of these effects. A total of 30 rats used in the study were randomly divided into 5 equal groups and the first group was kept as the control group. High-dose (100 mg/kg) or low-dose (20 mg/kg) favipiravir was administered alone or in combination with vitamin C (150 mg/kg) to other groups. Administration of both high and low doses of favipiravir significantly increased TBARS levels in brain tissue of aged rats. Similarly, both high and low doses of favipiravir led to significant increases in Bcl-2 and caspase-3 relative mRNA expression. However, only low dose favipiravir caused a significant increase in iNOS and IL-1ß relative mRNA expression levels. Similar results were also observed in histopathological examinations. However, co-administration of vitamin C with favipiravir attenuated some of the adverse effects of favipiravir. In conclusion, in this study, it was shown that the use of favipiravir caused some adverse effects through oxidative, inflammatory and apoptotic processes in the brain tissue of aged rats, and the potential of vitamin C to alleviate these effects.

The effect of vitamin C supplementation on favipiravir-induced oxidative stress and proinflammatory damage in livers and kidneys of rats.

Background: Favipiravir (FPV), an effective antiviral agent, is a drug used to treat influenza and COVID-19 by inhibiting the RNA-dependent RNA polymerase (RdRp) of RNA viruses. FPV has the potential to increase oxidative stress and organ damage. The purpose of this study was to demonstrate the oxidative stress and inflammation caused by FPV in the liver and kidneys of rats, as well as to investigate the curative effects of vitamin C (VitC).Methods: A total of 40 Sprague-Dawley male rats were randomly and equally divided into the following five groups: 1st; Control, 2nd; FPV = 20 mg/kg, 3rd; FPV = 100 mg/kg, 4th; FPV = 20 mg/kg + VitC (150 mg/kg), and 5th; FPV = 100 mg/kg + VitC (150 mg/kg) groups. Rats were given either FPV (orally) or FPV plus VitC (intramuscular) for 14 days. Rat blood, liver, and kidney samples were collected at 15 days to be analyzed for oxidative and histological changes.Results: FPV administration resulted in an increase in proinflammatory cytokines (TNF-α and IL-6) in the liver and kidney, as well as oxidative and histopathologic damage. FPV increased TBARS levels significantly (p < .05) and decreased GSH and CAT levels in liver and kidney tissues but had no effect on SOD activity. VitC supplementation significantly reduced TNF-a, IL-6, and TBARS levels while increasing GSH and CAT levels (p < .05). Furthermore, VitC significantly attenuated FPV-induced histopathological alterations associated with oxidative stress and inflammation in the liver and kidney tissues (p < .05).Conclusion: FPV caused liver and kidney damage in rats. In contrast, co-administration of FPV with VitC improved FPV-induced oxidative, pro-inflammatory, and histopathological changes.

Effects of fish oil on methotrexate-induced reproductive damage in rats.

Methotrexate (MTX) is a folic acid antagonist that is commonly used in paediatric and adult oncology to treat a variety of malignancies. Internal organs, including the testis, are severely cytotoxic and genotoxic to MTX. Omega-3, as an antioxidant, has been shown to protect rat testis tissue from injury. The effect of fish oil (FO) on MTX-induced reproductive damage in rats was investigated in this work. The 28 animals were divided into four groups for this purpose (control, FO, MTX, and MTX-FO). On the third day, the MTX group received a single intraperitoneal injection of 20 mg/kg MTX. Furthermore, in the FO and MTX-FO groups, FO was delivered through gavage once daily for 14 days. All animals euthanized under general anaesthesia on the 15th day. TBARS, catalase, glutathione peroxidase, glutathione (GSH), superoxide dismutase levels were measured biochemically. The Cosentino grading system was utilized for histology. Germ cell thickness and caspase-3 activity were also evaluated. In addition, sperm motility rate, epididymal sperm count, aberrant sperm rate, and sperm vitality were measured to assess sperm quality. Some TBARS levels have increased, but GSH levels decreased significantly in the MTX group. FO reduced TBARS levels while considerably increasing GSH levels. All sperm quality measures were significantly lowered in the MTX group, while FO had a recovery effect. There were no notable variations in histopathology across groups except for germ cell thickness, which reduced considerably in the MTX group and recovered with FO treatment. As a result, FO has been shown to reduce testicular toxicity following MTX treatment in rats.

Favourable effect of ß-glucan treatment against cisplatin-induced reproductive system damage in male rats.

The aim of this study was to investigate the potential beneficial effects of ß-glucan treatment against oxidative, histological and spermatological damage caused by cisplatin on the male reproductive system. Twenty-eight Sprague Dawley male rats were used in the study. The rats were randomly divided into four equal-sized groups: a control group, cisplatin group (7 mg/kg in a single-dose cisplatin administered intraperitoneally), ß-glucan group (ß-glucan given at a dose of 50 mg kg-1  d-1 for 14 day) and a cisplatin plus ß-glucan group (cisplatin and ß-glucan administered together at the same dose). Cisplatin administration induced an increase in the level of thiobarbituric acid-reactive substances, a lipid peroxidation indicator. It induced a decrease in enzymatic (superoxide dismutase, catalase and glutathione peroxidase) activities and nonenzymatic (reduced glutathione) antioxidant levels. In addition, cisplatin caused both histological and spermatological damage, as shown by a decrease in sperm motility and epididymal sperm concentrations and an increase in abnormal sperm rates. The ß-glucan treatment improved cisplatin-induced oxidative, histological and spermatological damage. This study revealed that ß-glucan treatment provided prevention against male reproductive system damage caused by cisplatin. These preventative effects were likely due to its antioxidant properties.

Beta-glucan attenuates cerebral ischemia/reperfusion-induced neuronal injury in a C57BL/J6 mouse model

Beta-glucans (ßg), that have many useful effects on human health, are natural polysaccharides. Our aim in this study was to determine useful effect of ßg against oxidative and neuronal damage caused by global cerebral ischemia/reperfusion (IR) in stroke imitated mice via surgical operation. A total of 40 mice divided into four equal groups randomly. The group 1 (sham operated) was kept as control. Bilateral carotid arteries of subjects in group 2 (I/R) and group 4 (I/ R + ßg) were clipped for 15 min, and the mice in group 4 (I/R + ßg) were treated with ßg (50 mg/kg/day), while the mice in group 2 (I/R) were treated with only vehicle for 10 days. The mice of group 3 (ßg) were treated with ßg for 10 days without carotid occlusion. Global cerebral I/R significantly increased oxidative stress and decreased members of anti-oxidant defense system. In addition, I/R caused histopathological damage in the brain tissue. However, ßg treatment ameliorated both oxidative and histopathological effects of I/R. Our present study showed that ßg treatment significantly ameliorated oxidative and histological damage in the brain tissue caused by cerebral I/R. Therefore, ßg treatment can be used as supportive care for ischemic stroke patients

Beneficial effects of ß-glucan against cisplatin side effects on the nervous system in rats 1.

PURPOSE: To investigate the protective effect of Bg on cisplatin (CP)-induced neurotoxicity in rats. METHODS: Twenty eight rats were randomly distributed into four groups. The first group was kept as a control. In the second group, CP was given at the single dose of 7 mg/kg intraperitoneally. In the third group, ßg was orally administered at the dose of 50 mg/kg/day for 14 days. In the fourth group, CP and ßg were given together at the same doses. RESULTS: CP treatment caused significant oxidative damage via induction of lipid peroxidation and reductions antioxidant defense system potency in the brain tissue. In addition, histopathological damage increased with CP treatment. On the other hand, ßg treatment largely prevented oxidative and histopathological negative effects of CP. CONCLUSIONS: Cisplatin has severe neurotoxic effects in rats and ßg supplementation has significant beneficial effects against CP toxicity depending on its antioxidant properties. Thus, it appears that ßg might be useful against CP toxicity in patients with cancer in terms of nervous system.

Hesperidin protects brain and sciatic nerve tissues against cisplatin-induced oxidative, histological and electromyographical side effects in rats.

In the present study, the beneficial effect of hesperidin (HP), a citrus flavonoid, on cisplatin (CP)-induced neurotoxicity was investigated. A total of 28 rats were equally divided into four groups; the first group was kept as control. In the second and third groups, CP and HP were given at the doses of 7 and 50 mg/kg/day, respectively. In the fourth group, CP and HP were given together at the same doses. The results indicated that although CP caused significant induction of lipid peroxidations and reduction in the antioxidant defense system potency in the brain and sciatic nerve, HP prevented these effects of CP. Besides, CP led to histopathological damage, mainly apoptosis, as well as electromyographical (EMG) changes in sciatic nerve. On the other hand, HP treatment reversed histopathological and EMG effects of CP. In conclusion, CP had severe dose-limiting neurotoxic effects and these effects of CP can be prevented by HP treatment. Thus, it appears that coadministration of HP with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.

Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity.

OBJECTIVE: The protective effects of fish oil (FO) on cisplatin (CP)-induced central and peripheral neurotoxicity were investigated in rats. METHODS: Rats (n = 28) were divided equally into four groups, the first group was kept as a control. In the second and third groups, CP and FO were given at doses of 7 mg/kg and 1 softgel/rat/day, respectively. In the fourth group, CP and FO were given together at the same doses. RESULTS: Although CP caused significant oxidative damage, via induction of lipid peroxidation and reduction in the antioxidant defense system potency, FO treatment largely reversed these effects. CP also resulted in histopathological damage, such as apoptosis, and electromyographical changes in the sciatic nerve. FO treatment partially prevented the histopathological and electromyographical effects of CP. DISCUSSION: CP has severe central and peripheral neurotoxic effects in rats and these effects were largely prevented by FO treatment. Thus, it appears that co-administration of FO with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.