Butterbur (Petasites hybridus) Extract Ameliorates Hepatic Damage Induced by Ovalbumin in Mice.

The liver is the most vital organ that could be influenced by inducers of hypersensitivity such as ovalbumin. The current study was carried out to explore the effects of butterbur (Petasites hybridus) extract on the ovalbumin-induced liver hypersensitivity in Swiss albino male mice. Animals were divided into 4 groups, 1st group served as a control group, 2nd group treated with daily oral administration of 75 mg/kg of butterbur extract, 3rd group received single oral dose 100 mg/kg of ovalbumin to induce hypersensitivity, and 4th group treated with oral administration of butterbur extract one-day post to the hypersensitivity induction. Ovalbumin induces a significant increase in the activity of liver enzymes and MDA and decreased the activity of CAT after the ovalbumin treatment. Histopathological investigations revealed marked pathological alterations in liver tissues in the form of hyaline degeneration and fibrosis. Additionally, heavy immune response indicated by immunostaining of MDA and TNF-α could be observed. In contrast, posttreatment with butterbur extract after hypersensitivity induction resulted in a significant decrease of liver enzymes and oxidative stress and reduced the inflammation and fibrosis of liver tissues. These results suggest that butterbur extract is considered as anti-inflammatory and antioxidant therapeutic herb for hypersensitivity treatment of liver.

Reno-protective effects of propolis on gentamicin-induced acute renal toxicity in swiss albino mice / Efectos renoprotectores del propóleo sobre la toxicidad renal aguda inducida por gentamicina en ratones albinos suizos

Antecedentes: El riñón es un órgano vital que desempeña una función importante e insustituible en la desintoxicación y la eliminación de los xenobióticos y, por lo tanto, es vulnerable a desarrollar diversas formas de lesión. Esto hace muy importante la búsqueda de compuestos renoprotectores naturales. Objetivos: Este estudio tiene como objetivo evaluar las propiedades renoprotectoras del propóleo contra la toxicidad renal inducida por gentamicina en ratones. Métodos: Para este estudio se utilizaron 3 grupos de 10 ratones macho en cada uno. El primer grupo sirvió como control, el segundo grupo (grupo Gm) recibió 80mg/kg de peso corporal de gentamicina por vía oral durante 7 días y el tercer grupo (grupo GmP) recibió la misma dosis de gentamicina con propóleo (500mg/kg de peso corporal) durante 7 días. Se utilizaron varios parámetros para estudiar la toxicidad renal. Resultados: La gentamicina causó daño renal significativo, como demostró el aumento de los niveles de nitrógeno ureico en sangre, la disminución de la hipocelularidad glomerular, los túbulos moderadamente dilatados y la pérdida leve del borde en cepillo, la infiltración grave, la degeneración tubular extensa y la presencia de cilindros tubulares. Los resultados de la histoquímica muestran presencia de colágeno y fibras reticulares. Las reacciones inmunohistoquímicas muestran lesión renal (expresión del gen Kim-1), estrés oxidativo (expresión del gen MDA) y un aumento de la apoptosis (expresión del gen caspasa-3). La administración concomitante de propóleo con gentamicina mostró disminución significativa de los niveles de nitrógeno ureico en la sangre, aspecto de glomérulos sanos con celularidad normal, reducción de la lesión tubular, disminución de colágeno y deposición de fibras reticulares, reducción de la apoptosis, daño renal y estrés oxidativo. Conclusión: Los resultados presentados en este estudio muestran claramente la función renoprotectora del propóleo contra la toxicidad inducida por gentamicina en el riñón de los ratones (AU)

Background: Kidney is a vital organ which plays an important and irreplaceable role in detoxification and removal of xenobiotics. And therefore is vulnerable to develop various forms of injuries. Hence, making it immensely important to search for natural reno-protective compounds. Objectives: This study therefore, aims to evaluate the reno-protective properties of propolis against gentamicin induced renal toxicity in mice. Methods: Three groups of 10 male mice each were used for this study. First group served as control, the second group (Gm group) was administered orally 80mg/kg body weight gentamicin for 7 days, and the third group (GmP group) was administered same dose of gentamicin with propolis (500mg/kg body weight) for 7 days. Various parameters were used to study the renal toxicity. Results: Gentamicin caused significant renal damage as evident by the rise in BUN levels, diminished glomeruli hypocellularity, moderately dilated tubules, and mild loss of brush border, severe infiltration, extensive tubular degeneration and presence of tubular cast. Histochemistry results show presence of collagen and reticular fibres. Immunohistochemical reactions show kidney injury (Kim-1 gene-expression), oxidative stress (MDA gene-expression), and an increase in apoptosis (caspase-3 gene-expression). Co-administration of propolis with gentamicin showed significant decrease in BUN levels, appearance of healthy glomeruli with normal cellularity, reduction of tubular injury, decrease of collagen and reticular fibres deposition, reduction of apoptosis, kidney injury and oxidative stress. Conclusion: Results presented in this study clearly show the reno-protective role of propolis against gentamicin-induced toxicity on mice kidney (AU)

Reno-protective effects of propolis on gentamicin-induced acute renal toxicity in swiss albino mice.

BACKGROUND: Kidney is a vital organ which plays an important and irreplaceable role in detoxification and removal of xenobiotics. And therefore is vulnerable to develop various forms of injuries. Hence, making it immensely important to search for natural reno-protective compounds. OBJECTIVES: This study therefore, aims to evaluate the reno-protective properties of propolis against gentamicin induced renal toxicity in mice. METHODS: Three groups of 10 male mice each were used for this study. First group served as control, the second group (Gm group) was administered orally 80mg/kg body weight gentamicin for 7 days, and the third group (GmP group) was administered same dose of gentamicin with propolis (500mg/kg body weight) for 7 days. Various parameters were used to study the renal toxicity. RESULTS: Gentamicin caused significant renal damage as evident by the rise in BUN levels, diminished glomeruli hypocellularity, moderately dilated tubules, and mild loss of brush border, severe infiltration, extensive tubular degeneration and presence of tubular cast. Histochemistry results show presence of collagen and reticular fibres. Immunohistochemical reactions show kidney injury (Kim-1 gene-expression), oxidative stress (MDA gene-expression), and an increase in apoptosis (caspase-3 gene-expression). Co-administration of propolis with gentamicin showed significant decrease in BUN levels, appearance of healthy glomeruli with normal cellularity, reduction of tubular injury, decrease of collagen and reticular fibres deposition, reduction of apoptosis, kidney injury and oxidative stress. CONCLUSION: Results presented in this study clearly show the reno-protective role of propolis against gentamicin-induced toxicity on mice kidney.

Attenuation of hepatotoxicity and oxidative stress in diabetes STZ-induced type 1 by biotin in Swiss albino mice.

Diabetes mellitus is one of the major health problems. This study was designed to investigate the effect of biotin to regulate blood glucose level, reduced toxicity and oxidative stress in liver of diabetic mice STZ-induced type 1. Male mice were divided into three groups, the first one served as the control group, the second and the third groups received single ip dose of 150 mg/kg of STZ, the second group served as the untreated diabetic group, the third group received daily oral dose of 15 mg/kg of biotin, livers and liver index showed insignificant difference among groups. Blood glucose level showed a significant decrease in treated diabetic mice compared to untreated diabetic mice. Biochemical analysis showed a significant decrease in liver enzymes AST and ALT compared to the control group. Histopathological examination showed severe changes in untreated diabetic liver tissue manifested by dilated portal vein, leukocytic infiltration, fatty degeneration and moderate to severe histopathological score, whereas, treated diabetic mice with biotin showed reduction in hepatotoxicity represented by appearance of relative healthy hepatocytes and normal histopathological score. Immunohistochemistry of acrolein showed intense immunoreactions in liver section of untreated diabetic mice and faint immunoreactions in treated diabetic mice with biotin as evidence to oxidative stress reduction.

Pattern of neurobehavioral and organ-specific toxicities of ß, ß'-iminodipropionitrile in mice.

INTRODUCTION: ß, ß'-iminodipropionitrile (IDPN) is a synthetic nitrile that produces a permanent movement disorder in rodents. Although IDPN-induced vestibular pathology is well documented, the mode of IDPN interaction with other organ systems is poorly understood. We examined the behavioral signs and histopathological changes in the vestibular labyrinth, brain, liver and kidneys of mice exposed to IDPN. MATERIAL AND METHODS: Adult male SWR/J mice were divided into 2 groups of 6 animals each. One group of mice received normal saline (control group) and the other group was treated with IDPN (400 mg/kg, i.p.) daily for 7 days. Dyskinetic movements including vertical and horizontal head weaving, circling and backward walking were quantified on days 7, 8 and 9. RESULTS: We observed a direct correlation between the severity of IDPN-induced behavioral deficits and the degeneration of vestibular hair cells in the crista ampullaris of mice. The brain cortex of both groups appeared similar, whereas the kidney histopathology revealed mild nephrotoxicity in some of the IDPN-treated mice. Administration of IDPN caused severe hepatotoxicity, but the intensity of hepatic damage was not correlated with the severity of behavioral deficits. CONCLUSIONS: Degeneration of vestibular sensory hair cells plays an important role in the development of IDPN-induced behavioral deficits in mice. Exposure to IDPN also caused severe hepatotoxicity which was independent of the behavioral symptoms. These findings could be of potential relevance to human health, particularly after the observation that IDPN not only causes a movement disorder but also produces acute liver injury.

Histological insights in iminodipropionitrile-induced toxicity in rats.

Iminodipropionitrile (IDPN) is a prototype nitrile compound that produces excitation, chorea and circling (ECC) syndrome in rodents. Previous studies have implicated vestibular hair cell degeneration in IDPN-induced behavioral abnormalities. Although the pathological changes in vestibular labyrinth of IDPN-treated rats are well documented, the effects of IDPN on other organ systems are not clearly understood. We therefore examined the histopathological alterations in inner ear, brain, liver and kidneys of rats exposed to IDPN. Adult male Wistar rats were divided into two groups of six animals each. Control rats received normal saline whereas the IDPN group was treated with IDPN (100mg/kg, i.p.) daily for 7 days. All the animals were carefully observed for any behavioral abnormality and the dyskinetic movements including the vertical and horizontal head weaving, circling and backward walking were quantified. The animals were sacrificed on day 9 and the samples of cochlea, brain, liver and kidney were collected for histopathology. The results showed a direct correlation between the severity of behavioral deficits and the cellular damage in crista ampullaris in IDPN-treated rats. Histopathology of liver was severely influenced by IDPN treatment, leading to vacuolization of cytoplasm, distorted sinusoids, infiltration of mononuclear cells and necrotic zones. However, the severity of hepatic damage in IDPN-treated rats was independent of the magnitude of vestibular hair cell degeneration as well as the severity of behavioral deficits. Administration of IDPN in the vestibulotoxic doses did not produce any histological changes in the brain cortex and kidneys of rats.