Development and validation of analytical methods for the simultaneous estimation of Nimorazole and Ofloxacin in tablet dosage form

Two simple, rapid, accurate and precise spectrophotometric methods have been developed for simultaneous estimation of Nimorazole and Ofloxacin from tablet dosage form. Method І involves formation of ‘simultaneous equations’ at 304 nm (λ max of Nimorazole) and 287.5 nm (λ max of Ofloxacin); while Method ІІ involves, formation of ‘Absorbance ratio equation’ at 301(isoabsorptive point) and 287.5 nm (λ max of Ofloxacin) using distilled water as a solvent. The linearity was observed in the concentration range of 5 - 25 μg/ml for Nimorazole and 2 - 10 μg/ml for Ofloxacin. The results of analysis have been validated statistically and by recovery studies and were found satisfactory

Convergent Transcription of Interferon-stimulated Genes by TNF-α and IFN-α Augments Antiviral Activity against HCV and HEV

IFN-\xce\xb1 has been used for decades to treat chronic hepatitis B and C, and as an off-label treatment for some cases of hepatitis E virus (HEV) infection. TNF-\xce\xb1 is another important cytokine involved in inflammatory disease, which can interact with interferon signaling. Because interferon-stimulated genes (ISGs) are the ultimate antiviral effectors of the interferon signaling, this study aimed to understand the regulation of ISG transcription and the antiviral activity by IFN-\xce\xb1 and TNF-\xce\xb1. In this study, treatment of TNF-\xce\xb1 inhibited replication of HCV by 71 \xc2\xb1 2.4% and HEV by 41 \xc2\xb1 4.9%. Interestingly, TNF-\xce\xb1 induced the expression of a panel of antiviral ISGs (2-11 fold). Blocking the TNF-\xce\xb1 signaling by Humira abrogated ISG induction and its antiviral activity. Chip-seq data analysis and mutagenesis assay further revealed that the NF-\xce\xba B protein complex, a key downstream element of TNF-\xce\xb1 signaling, directly binds to the ISRE motif in the ISG promoters and thereby drives their transcription. This process is independent of interferons and JAK-STAT cascade. Importantly, when combined with IFN-\xce\xb1, TNF-\xce\xb1 works cooperatively on ISG induction, explaining their additive antiviral effects. Thus, our study reveals a novel mechanism of convergent transcription of ISGs by TNF-\xce\xb1 and IFN-\xce\xb1, which augments their antiviral activity against HCV and HEV

Monitoring of Interferon Response Triggered by Cells Infected by Hepatitis C Virus or Other Viruses Upon Cell–Cell Contact

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