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Background: Tramadol hydrochloride/paracetamol (THP) a fixed dose combination (FDC) is widely spread analgesic used to treat moderate to moderately severe pain. Over dose or chronic use of this fixed dose combination produce serious adverse effects. An acute Tramadol hydrochloride/paracetamol (THP) overdose can lead to a fatal liver damage. Objectives: There is a worldwide need to develop a safe and symptomatic medication which controls the different medical complications. Materials and Methods: Healthy adult swiss albino mice were assigned to four groups of six mice each according to their weights. Group-I serve as control, Group-II received Multi herbal formulation (AKSS16 LIV01) 400 mg/kg/day, Group-III received Tramadol hydrochloride/paracetamol (THP) 1.68 g / 300ml water and Group-IV received THP along with AKSS16-LIV01 (400 mg/kg). Blood samples were collected from the retro orbital plexus of each animal to determine various blood parameters and liver transaminase. Results: Administration of THP showed decline body weight, food consumption and water intake in mice whereas treatment with Multi herbal formulation (AKSS16-LIV01) normalized the same as compared with untreated animals. Treatment with THP (Group-III) decline the packed cell volume (PCV), haempglobin (Hb), means cell volume (MCV), means cell hemoglobin (MCH) and greater the white blood cell (WBC) compared with control. Pre-treatment with AKSS16-LIV01 significantly (p

Background: Hepatotoxicity is one of the common side effects of nonsteroidal anti-inflammatory drugs (NSAIDs). Scientific study stated that hepatotoxicity is the most serious adverse effects of Aceclofenac. Objectives: In this study, our aim was to investigate the use of Fortibile® tablet containing ursodeoxycholic acid (UDCA) in prevention of the hepatotoxic effect and biochemical changes induced by aceclofenac (ACE) in laboratory mice. Materials and Methods: Swiss albino mice were divided into four groups (control, UDCA (Fortibile® tablet) 20 mg/kg, aceclofenac (ACE) 50mg/kg, UDCA 20 mg/kg + aceclofenac 50 mg/kg). Results: Administration of aceclofenac (ACE) showed decline body weight, food consumption, water intake and elevated liver weight in mice whereas treatment with UDCA (Fortibile® tablet) normalized the same as compared with untreated animals. Animals treated with aceclofenac caused elevated activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) as well as total and direct bilirubin level. These elevations in liver enzymes were decreased by combination of aceclofenac with UDCA. On the other hand application of aceclofenac (ACE) on mice caused a significant increase in serum and tissue malondialdehyde (MDA) and nitric oxide (NO) content but significant decrease in glutathione GSH and GPx content. Combine thepary of UDCA and aceclofenac resulted in a significant decrease in MDA, NO content and significantly elevated GSH and GPx content. Conclusion: It could be concluded that Fortibile® tablet containing Ursodeoxycholic acid acts as an effective hepatoprotective agent against NSAIDs induced liver dysfunction, and this effect might be related to its antioxidant properties. Hepatic functions should be monitored, and the dose should be adjusted during aceclofenac (ACE) therapy. Keywords: Ursodeoxycholic acid, Aceclofenac, Hepatotoxicity, Liver function test, Oxidative stress

Arsenic toxicity is one of the major environmental problems causing various diseases, cardiovascular disorders is one of them. Several epidemiological studies have shown that arsenic causes cardiac hypertrophy but the detailed molecular mechanism is to be studied yet. This study is designed to determine the molecules involved in the augmentation of arsenic-induced cardiac hypertrophy. Furthermore, the effects of oleic acid on arsenic-induced hypertrophy and cardiac injury have also been investigated. Our results show that arsenic induces cardiac hypertrophy both in vivo in mice and in vitro in rat H9c2 cardiomyocytes. Moreover, arsenic results in decreased activity of AMPK and FoxO1 along with increased NFATc3 expression, a known cardiac hypertrophy inducer. In addition, activation of AMPK and FoxO1 results in reduced NFATc3 expression causing attenuation of arsenic-induced cardiac hypertrophy in H9c2 cells. Interestingly, we have observed that oleic acid helps in ameliorating cardiac hypertrophy in arsenic-exposed mice. Our studies on protection from arsenic-induced cardiac hypertrophy by oleic acid in H9c2 cells shows that oleic acid activates AMPK along with increased nuclear FoxO1 localization, thereby reducing NFATc3 expression and attenuating cardiomyocyte hypertrophy. This study will help in finding out new avenues in treating arsenic-induced cardiac hypertrophy.