The protective effects of baicalin and chrysin against emamectin benzoate-induced toxicity in Wistar albino rats.

The aim of this study was to investigate the effects of baicalin, chrysin and their combinations against emamectin benzoate-induced toxicity in rats. For this purpose, sixty four rats were divided into evenly 8 groups with 6-8-week-old male Wistar albino rats, weighing 180-250 g, in each group. While the first group was kept as a control (corn oil), the remaining 7 groups were administered with emamectin benzoate (10 mg/kg bw), baicalin (50 mg/kg bw) and chrysin (50 mg/kg bw) alone or together for 28 days. Oxidative stress parameters, serum biochemical parameters and blood/tissue (liver, kidney, brain, testis and heart) and tissue histopathology were investigated. Compared to the control group, the emamectin benzoate-intoxicated rats had significantly higher tissue/plasma concentrations of nitric oxide (NO) and malondialdehyde (MDA), as well as lower tissue glutathione (GSH) concentrations and antioxidant enzyme activity (glutathione peroxidase/GSH-Px, glutathione reductase/GR, glutathione-S-transferase/GST, superoxide dismutase/SOD, catalase/CAT). Biochemical analysis showed that emamectin benzoate administration significantly increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) activities, as well as triglyceride, cholesterol, creatinine, uric acid and urea levels, and decreased serum total protein and albumin levels. The histopathological examination of the liver, kidney, brain, heart and testis tissues of the emamectin benzoate-intoxicated rats demonstrated necrotic changes. Baicalin and/or chrysin reversed the biochemical and histopathological alterations induced by emamectin benzoate on these tested organs. Therefore, baicalin and chrysin (alone or in combination) could offer protection against emamectin benzoate-induced toxicity.

The protective effect of chrysin against oxidative stress and organ toxicity in rats exposed to propetamphos.

The aim of this study was to investigate the protective efficacy of chrysin against propetamphos exposure. For this purpose, 2 to 3-month-old 40 male Wistar Albino rats were used. These animals were randomly assigned to four groups. The animals in the control group received the vehicle substance (corn oil) alone. Groups 2, 3 and 4 were administered with 50 mg/kg.bw/day of chrysin (in corn oil), 10 mg/kg.bw/day of propetamphos (in corn oil), and 10 mg/kg.bw/day of propetamphos plus 50 mg/kg.bw/day of chrysin, respectively, for 28 days. Some oxidative stress/lipid peroxidation parameters (MDA, SOD, CAT, GSH-Px, NO, glutathione) and serum biochemical parameters (triglyceride, cholesterol, creatinine, BUN, creatine phosphokinase, ALT, ALP and pseudocholinesterase) were analyzed in tissue/blood samples. Also, histopathological findings were observed. According to the data obtained, no significant alteration had occurred in these parameters and the histological findings in the group given chrysin alone, when compared to the control group. Significant unfavorable alterations were detected in the oxidative stress/lipid peroxidation/antioxidant status parameters, all biochemical parameters and histopathological findings of the group that received propetamphos alone. In the group that was given both chrysin and propetamphos, remedial/recovery alterations were observed in the oxidative stress/lipid peroxidation/antioxidant status values, serum biochemical parameters and histopathological findings, such that the values and histopathological findings showed partly similarity to those of the control group. In result, it is suggested that chrysin may provide protection against propetamphos exposure and propetamphos-induced organ damage in rats at a certain level.

Effect of diosmin on lipid peoxidation and organ damage against subacute deltamethrin exposure in rats.

The aim of this study was to investigate the protective efficacy of diosmin against subacute deltamethrin exposure. For this purpose, 40 male Wistar albino rats were used. The animals were assigned to the following 4 groups: control group (received corn oil vehicle alone), diosmin-treated group (50 mg/kg bw/day orally), deltamethrin-exposed group (5 mg/kg bw/day, orally) and coadministered group (5 mg/kg bw/day deltamethrin and 50 mg/kg bw/day diosmin, orally) for 28 days. Some lipid peroxidation/antioxidant status/biochemical markers were evaluated in blood/tissue (liver, kidney, brain, heart and testis) samples and the histopathological architecture was assessed. Compared with the control group, no alteration was detected in the parameters and histological findings of the diosmin-treated group. Deltamethrin toxicity was associated with significantly increased plasma, cardiac, hepatic, renal, cerebral and testicular levels of MDA and NO, and significantly decreased GSH levels (p < 0.05). Antioxidant enzyme status (SOD, CAT and GSH-Px activities) displayed either decrease or increase (p < 0.05). Significant increase was detected in AST and ALT activities and urea and creatinine levels (p < 0.05). The values of the group coadministered with deltamethrin and diosmin were similar to the values of the control group. Diosmin ameliorated deltamethrin-induced lymphocytic and histiocytic infiltration and subendocardial oedema in the heart. Combined administration also minimized hepatic, renal, testicular and cerebral histopathological findings. The alterations detected in various toxicological parameters correlated well with the histopathological changes observed in various organs. In conclusion, it is suggested that diosmin could provide protection against deltamethrin-induced toxicity and organ damage in rats.

The effects of chrysin on lipopolysaccharide-induced sepsis in rats.

Chrysin (CR) is a flavone found in propolis and many plants. Lipopolysaccharide (LPS) is a component of the cell wall of gram-negative bacteria that causes sepsis. The purpose of this study was to investigate the effects of CR on LPS-induced sepsis in rats. LPS intraperitoneal and a single dose and CR were given orally for 10 days. Rats were sacrificed, blood samples were taken, liver, lung, and kidney tissues were dissected, homogenized, and histopathological analysis was carried out. When CR groups compared to sepsis group, CR significantly decreased the serum levels of aspartate transaminase (AST) and alanine aminotransferase (ALT), interleukin-1 beta (IL-1ß), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and levels of malondialdehyde (MDA) in tissues. CR also increased the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in tissues. Histopathological findings were consistent with biochemical findings. Conclusion, CR could reduce the oxidative stress markers and cytokines in sepsis. PRACTICAL APPLICATIONS: Our approach is to determine the antioxidant and anti-inflammatory effects of chrysin, known as a flavolonoid, which are found in many plants and foods such as honey and propolis. In this study, experimental sepsis model was created using LPS. According to the results of the study, CR can attribute to the ameliorating of oxidative damage in tissues (lung, liver, and kidney) and it can suppress the sepsis-associated acute tissue injury via reduction of inflammation in rats. Even, CR can be used as a pharmacological agent in inflammatory diseases caused by other sources and in many cases causing oxidation.

The effects of colostrum on some biochemical parameters in the experimental intoxication of rats with paracetamol.

In the current study, the possible prophylactic and therapeutic effects of colostrum (COL) on acute organ injury caused by paracetamol (PAR) in rats were evaluated. Within the scope of this study, a 2-month-old male (150-200 g) 70 Wistar Albino rat was used and a total of seven groups were designed. The first group (CNT) was maintained for control purposes. The second group (COL-1) was given COL for 1 day, at a dose of 500 mg/kg at 6-h intervals, and blood and tissue sampling was performed at 24 h. The third group (COL-7) received COL for 7 days, at a dose of 500 mg/kg at 6-h intervals on day 1 and at a daily dose of 500 mg/kg on the following days, and blood and tissue samples were taken at the end of seventh day. The fourth group (PAR-1) was administered with PAR at a dose of 1.0 g/kg bw and was blood and tissue sampled at 24 h. The fifth group (PAR-7) received PAR at a dose of 1.0 g/kg bw on day 1 and was blood and tissue was removed at the end of day 7. The sixth group (PAR+COL-1) was administered with a combination of PAR (1 g/kg bw) and COL (500 mg/kg at 6-h intervals), and blood and tissue samples were collected at 24 h. The seventh group (PAR+COL-7) received 1.0 g/kg bw of PAR on day 1 and was given COL throughout the 7-day study period (at a dose of 500 mg/kg at 6-h intervals on day 1 and at a daily dose of 500 mg/kg on the following days). In the seventh group, blood and tissue samples were taken at the end of seventh day. Alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), glucose, creatinine, triglyceride, total bilirubin, total protein and albumin levels/activities were analysed in the serum samples. The malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) levels/activities, known as oxidative stress parameters, were assayed for tissue homogenates and blood (erythrocytes/plasma); in addition, enzyme activities of GSH S-transferase (GST), cytochrome P4502E1 (CYP2E1), NADH-cytochrome b5 reductase (CYTB5), glucose-6-phosphate dehydrogenase (G6PD), NADPH-cytochrome P450 C reductase (CYTC) and glutathione (GSH) levels/activities defined as drug metabolising parameters were measured in liver homogenates. In result, it was determined that PAR caused significant alterations in some biochemical and lipid peroxidation parameters and the activities/levels of drug metabolising parameters in the liver and that COL normalised some of these parameters and reduced PAR-induced tissue damage.

The effects of diosmin on aflatoxin-induced liver and kidney damage.

Aflatoxin is among the natural toxins that cause serious side effects on living things. Diosmin is also one of the compounds with broad pharmacological effects. In this study, the effects on the oxidant/antioxidant system of 50 mg/kg body weight/day dose of diosmin, aflatoxin (500 µg/kg body weight/day), and combined aflatoxin (500 µg/kg body weight/day) plus diosmin (50 mg/kg body weight/day) given to the stomach via catheter female adult Wistar Albino rats is examined. Forty rats were used in the experiment, and these animals were randomly allocated to four equal groups. The test phase lasted 21 days, and blood samples and tissue (liver and kidney) samples were taken after this period was over. Some biochemical parameters (glucose, triglyceride, cholesterol, blood urea nitrogen, creatinine, uric acid, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total protein, albumin) and levels of malondialdehyde, nitric oxide, and 4-hydroxynonenal and activities of superoxide dismutase, catalase, and glutathione peroxidase were analyzed in the samples. The aflatoxin administered over the period indicated a significant increase in levels of malondialdehyde (MDA), nitric oxide (NO), and 4-hydroxynonenal (4-HNE) in all tissues and blood samples. Therewithal, the activity of antioxidant enzymes showed a change in the decreasing direction. Biochemical parameters of the group in which aflatoxin were administered alone changed unfavorably. Parallel effects were also observed in the histopathological findings of this group. The results showed that aflatoxin changed antioxidant/oxidant balance in favor of oxidant and eventually led to lipid peroxidation. Diosmin administration to aflatoxin-treated animals resulted in positive changes in antioxidant enzyme activities while the levels of MDA, NO, and 4-HNE were reduced in all tissues and blood samples examined. Diosmin alleviates the oxidative stress caused by aflatoxin. Similar improvement was observed in biochemical parameters of this group as well as in liver and kidney histopathology. No significant change was observed in the group treated with diosmin alone in terms of the parameters examined and histologic findings. As a result, diosmin may be included in compounds that can be used as a therapeutic and prophylactic agent in the event of the formation of aflatoxin exposure and poisoning in animals.