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Context Ficus recemosa Linn. (Moraceae) has been reported as a natural folk medicine with diverse pathological activities such as antioxidant, antidiabetic, renoprotective and cardioprotective. Objective The present study evaluates the preventive effect of standardised ethanol extract of F. racemosa stem bark (EEFSB) on diabetic cardiomyopathy (DC) and diabetic nephropathy (DN). Materials and methods Animals were rendered diabetic by one time administration of STZ (45 mg kg(-1), i.v.) and, after 7 d, diabetic rats were randomised into four groups of eight rats each. EEFSB (200 and 400 mg kg(-1)) was administered to diabetic rats once daily for 8 weeks. Furthermore, the presence of phytochemicals was evaluated by HPTLC. Results Treatment with EEFSB markedly restores the blood glucose and lipid level (p < 0.001), also reduced creatinine kinase (p < 0.001), lactate dehydrogenase (p < 0.001), C-reactive protein (p < 0.001), creatinine (p < 0.001), blood urea nitrogen (p < 0.001), collagen (p < 0.05) and albumin (p < 0.001) levels. Reduced level of sodium (p < 0.001), creatinine (p < 0.001), albumin (p < 0.001) and malondialdehyde (p < 0.01) in heart and kidney tissue along with enhanced activities of superoxide dismutase (p < 0.001) and reduced glutathione (p < 0.001). Moreover, left ventricular hypertrophic index and cardiac hypertrophic index were markedly reduced by EEFSB treatment. Conclusion The findings of this study provided strong scientific evidence for the traditional use of F. racemosa and postulate protective effects against diabetes and its complications such as DC and DN.

Azithromycin (AZI) is a semi-synthetic macrolide antibiotic drug, effective against a wide variety of bacteria. The present study describes a simple, accurate, reproducible and precise UV Spectrophotometric method for the estimation of AZI (pH 6.8 Phosphate buffer). The absorbance maximum (λ max ) for AZI was found to be 208nm. The method reveals high sensitivity, with linearity in the 10 µg/ml to 50 µg/ml range. The lower limit of detection was found to be 1.6µg/ml and the limit of quantification was found to be 5µg/ml. All the calibration curves demonstrated a linear relationship between the absorbance and concentration, with the correlation coefficient higher than 0.99. The % recovery was found to be 99.72%. AZI was also subjected to stress degradation under different conditions recommended by the International Conference on Harmonization (ICH). Introduction:

Parkinson's disease (PD) is a neurodegenerative disorder that affects 2%–3% of the population worldwide. Clinical presentation of PD includes motor and non‐motor symptoms. The interplay between pathogenic factors such as increased oxidative stress, neuroinflammation, mitochondrial dysfunction and apoptosis are responsible for neurodegeneration in PD. Intrastriatal administration of 6‐hydroxy dopamine (6‐OHDA) in rat brain provoked oxidative and nitrosative stress by decreasing endogenous antioxidants such as superoxide dismutase, catalase, glutathione, glutathione peroxidase and glutathione reductase. Consequently, interleukin‐6, tumour necrosis‐α, interferon‐γ and cyclooxygenase‐2 mediated neuroinflammation leads to mitochondrial dysfunction, involving inhibition of complex‐II and IV activities, followed by apoptosis and degeneration of striatal dopaminergic neurons. Degeneration of dopaminergic neurons resulted in reduced dopamine turnover, consequently induced behavioural abnormalities in rats. Activation of peroxisome proliferator‐activated receptors (PPARs) have protective role in PD by modulating response of antioxidant enzymes, neuroinflammation and apoptosis in various animal models of PD. Saroglitazar (SG) being dual PPAR‐α/γ agonist activates both PPAR‐α and PPAR‐γ receptors and provide neuroprotection by reducing oxidative stress, neuroinflammation, mitochondrial dysfunction and apoptosis of dopaminergic cells in 6‐OHDA induced PD in rats. Thereby, SG restored striatal histopathological damage and dopamine concentration in rat striatum, and behavioural alterations in rats. Thus, SG proved neuroprotective effects in rat model of PD. Potential benefits of SG in rat model of PD advocates to consider it for further preclinical and clinical evaluation.