HPV16-positive cervical cancer lesions contain NFκB–ERα nuclear complexes to repress the TLR9 promoter.

Humans have been using natural products for medicinal use for ages. Natural products of therapeutic importance are compounds derived from plants, animals, or any microorganism. Ginger is also one of the most commonly used condiments and a natural drug in vogue. It is a traditional medicine, having some active ingredients used for the treatment of numerous diseases. During recent research on ginger, various ingredients like zingerone, shogaol, and paradol have been obtained from it. Zingerone (4-(4-hydroxy-3-methoxyphenyl)-2-butanone) is a nontoxic and inexpensive compound with varied pharmacological activities. It is the least pungent component of Zingiber officinale. Zingerone is absent in fresh ginger but cooking or heating transforms gingerol to zingerone. Zingerone closely related to vanillin from vanilla and eugenol from clove. Zingerone has potent anti-inflammatory, antidiabetic, antilipolytic, antidiarrhoeic, antispasmodic, and so forth properties. Besides, it displays the property of enhancing growth and immune stimulation. It behaves as appetite stimulant, anxiolytic, antithrombotic, radiation protective, and antimicrobial. Also, it inhibits the reactive nitrogen species which are important in causing Alzheimer's disease and many other disorders. This review is written to shed light on the various pharmacological properties of zingerone and its role in alleviating numerous human and animal diseases.

⌬Np73␣, a dominant-negative inhibitor of p53 and p73, exhibits antiapoptotic and transforming activity in in vitro models and is often found to be upregulated in human cancers. The mechanisms involved in the regulation of ⌬Np73␣ protein levels in normal and cancer cells are poorly characterized. Here, we show that that IB kinase beta (IKK␤) increases ⌬Np73␣ protein stability independently of its ability to activate NF-B. IKK␤ associates with and phosphorylates ⌬Np73␣ at serine 422 (S422), leading to its accumulation in the nucleus, where it binds and represses several p53-regulated genes. S422A mutation in ⌬Np73␣ abolished IKK␤-mediated stabilization and inhibition of p53-regulated gene expression. Inhibition of IKK␤ activity by chemical inhibitors, overexpression of dominant-negative mutants, or gene silencing by siRNA also resulted in ⌬Np73␣ destabilization, which under these conditions was rapidly translocated into the cytoplasm and degraded by a calpain-mediated mechanism. We also present evidence for the IKK␤ and ⌬Np73␣ cross talk in cancer-derived cell lines and primary cancers. Our data unveil a new mechanism involved in the regulation of the p73 and p53 network.p53 and its family members, p63 and p73, are transcription factors that play an important role in the regulation of the cell cycle, apoptosis, and cancer development (4, 23). All three proteins show similarity in the amino acid sequences of their N-terminal transcription activation (TA), DNA binding, and oligomerization domains. p73 and p53 are also functionally related, since they have the ability to bind a similar set of p53 regulatory elements (REs) (16). Both proteins are functionally regulated by posttranslational modifications, and p73 appears to be subject to more complex regulatory mechanisms than p53 at transcriptional level. The p73 gene is expressed as multiple isoforms that differ in their N and/or C terminus. The generation of different transcripts of p73 involves the use of two distinct promoters (P1 and P2) and/or alternative splicing. The mRNA of the full-length p73 isoform (TAp73) is transcribed by the P1 promoter located upstream of exon 1, while an isoform called ⌬Np73 is generated by using the P2 promoter in intron 3 (P2). Three additional ⌬ isoforms, ⌬NЈp73, ⌬Ex2p73, and ⌬Ex2/3p73, arise from alternative splicing of the transcripts originating from the first exons. All ⌬N isoforms lack the TA domain located at the N terminus (exons 2 and 3). Multiple splicing of exons 10 to 14 generate additional TA and

Nadeem M., Abdullah M., Hussain I., Inayat S., Javid A., Zahoor Y. (2013): Antioxidant potential of Moringa oleifera leaf extract for the stabilisation of butter at refrigeration temperature. Czech J. Food Sci., 31: 332-339.The antioxidant potential of a leaf extract of Moringa oleifera Lam. (Moringaceae) -LEMO was studied for the stabilisation of butter at refrigeration temperature. LEMO was obtained by extracting the ground and dried leaves with 80% ethanol at room temperature for 48 hours. LEMO was added into butter at three different concentrations, i.e. 400 ppm (T 1 ), 600 ppm (T 2 ), and 800 ppm (T 3 ) and compared with a treatment which was not supplemented with LEMO, i.e. control (T 0 ). The addition of LEMO at all three levels did not have any effect on butter composition. Free fatty acids, peroxide value and p-anisidine value (AnV) of T 2 after 90 days of storage were 0.10%, 0.71 meq/kg and 14.85 as compared to the control 0.16%, 1.24 meq/kg and 28.85, respectively. Peroxide value of the control and T 2 in Schaal oven test after 5 days in oven was 8.19 and 2.99 meq/kg, respectively. Induction period and overall acceptability score of the control and T 2 were 6.35 h, 8.91 h and 7.6, 7.2, respectively. The results of this study suggest that LEMO at 600 ppm may be used for reasonable storage stability of butter at refrigeration temperate with acceptable sensory characteristics.

Colon cancer is a world-wide health problem and one of the most dangerous type of cancer, affecting both men and women. Naringenin (4, 5, 7-trihydroxyflavanone) is one of the major flavone glycoside present in citrus fruits. Naringenin has long been used in Chinese's traditional medicine because of its exceptional pharmacological properties and non-toxic nature. In the present study, we investigated the chemopreventive potential of Naringenin against 1,2-dimethyhydrazine (DMH)-induced precancerous lesions, that is, aberrant crypt foci (ACF) and mucin depleted foci (MDF), and its role in regulating the oxidative stress, inflammation and hyperproliferation, in the colon of Wistar rats. Animals were divided into five groups. In groups 3-5, Naringenin was administered at the dose of 50 mg/kg b. wt. orally while in groups 2-4, DMH was administered subcutaneously in the groin at the dose of 20 mg/kg b. wt. once a week for first 5 weeks and animals were euthanized after 10 weeks. Administration of Naringenin ameliorated the development of DMH-induced lipid peroxidation, ROS formation, precancerous lesions (ACF and MDF) and it also reduced the infiltration of mast cells, suppressed the immunostaining of NF-κB-p65, COX-2, i-NOS PCNA and Ki 67 Naringenin treatment significantly attenuated the level of TNF-α and it also prevented the depletion of the mucous layer. Our findings suggest that Naringenin has strong chemopreventive potential against DMH-induced colon carcinogenesis but further studies are warranted to elucidate the precise mechanism of action of Naringenin.