@article {720, title = {Antiproliferative property of n-hexane and chloroform extracts of Anisomeles malabarica (L). R. Br. in HPV16-positive human cervical cancer cells.}, journal = {J Pharmacol Pharmacother}, volume = {3}, year = {2012}, month = {2012 Jan}, pages = {26-34}, abstract = {

OBJECTIVES: To find the efficacy of serial extracts of Anisomeles malabarica in inhibiting proliferation of and inducing apoptosis in human cervical cancer cells, SiHa and ME 180, that are HPV 16-positive.

MATERIALS AND METHODS: The whole plant was extracted in n-hexane, chloroform, ethyl acetate, n-butanol, methanol, and water. The cells were treated with the extracts at increasing concentrations to find the IC(50), adopting MTT ([3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide]) assay. Acridine orange (AO) and ethidium bromide (EB) and Hoechst 33258 staining were adopted to assess the mode of cell death, Annexin V-Cy3 staining to evaluate one of the early apoptotic features, JC-1 staining to assess the mitochondrial membrane depolarization, comet assay for DNA fragmentation, and cell cycle analysis for the distribution of cells after treatment.

RESULTS: n-Hexane and chloroform extracts were cytotoxic to the cervical cancer cells in dose- and duration-dependent manner. The cells that responded to the treatments revealed typical apoptotic features. Early features of apoptosis, phosphatidyl serine translocation and loss of mitochondrial trans-membrane potential, were observed in the treated cells, and comet assay revealed DNA damage. In the FACS analysis, the cells accumulated in the sub-G0/G1 phase of the cell cycle, except in n-hexane- and chloroform extract-treated SiHa cells at 24 h, which showed arrest in S- and G2/M phases.

CONCLUSIONS: n-Hexane and chloroform extracts of A. malabarica inhibit proliferation of and induce death in HPV16-positive cervical cancer cells, mostly by apoptosis and to some extent by necrosis.

}, issn = {0976-5018}, doi = {10.4103/0976-500X.92500}, author = {Preethy, Christo Paul and Padmapriya, Ramamoorthy and Periasamy, Vaiyapuri Subbarayan and Riyasdeen, Anvarbatcha and Srinag, Suresh and Krishnamurthy, Hanumanthappa and Alshatwi, Ali Abdullah and Akbarsha, Mohammad Abdulkader} } @article {724, title = {Neutrophil extracellular traps contain mitochondrial as well as nuclear DNA and exhibit inflammatory potential.}, journal = {Cytometry A}, volume = {81}, year = {2012}, month = {2012 Mar}, pages = {238-47}, abstract = {

Neutrophils expel extracellular traps (NETs) to entrap and exterminate the invaded micro-organisms. Acute/chronic inflammatory disorders are often observed with aberrantly enhanced NETs formation and high nitric oxide (NO) availability. Recent study from this laboratory demonstrated release of NETs from human neutrophils following treatment with SNP or SNAP. This study is an extension of our previous finding to explore the extracellular bacterial killing, source of DNA in the expelled NETs, their ability to induce proinflammatory cytokines release from platelets/THP-1 cells, and assessment of NO-mediated free radical formation by using a consistent NO donor, DETA-NONOate. NO-mediated NETs exhibited extracellular bacterial killing as determined by colony forming units. NO-mediated NETs formation was due to the activation of NADPH oxidase and myeloperoxidase. NO- or PMA-mediated NETs were positive for both nuclear and mitochondrial DNA as well as proteolytic enzymes. Incubation of NETs with human platelets enhanced the release of IL-1β and IL-8, while with THP-1 cells, release of IL-1β, IL-8, and TNFα was observed. This study demonstrates that NO by augmenting enzymatic free radical generation release NETs to promote extracellular bacterial killing. These NETs were made up of mitochondrial and nuclear DNA and potentiated release of proinflammatory cytokines.

}, keywords = {Adult, Blood Platelets, DNA, DNA, Mitochondrial, Free Radicals, Humans, Inflammation, Interleukin-1beta, Interleukin-8, Mitochondria, NADPH Oxidases, Neutrophil Activation, Neutrophils, Nitric Oxide, Peroxidase, Tumor Necrosis Factor-alpha}, issn = {1552-4930}, doi = {10.1002/cyto.a.21178}, author = {Keshari, Ravi S and Jyoti, Anupam and Kumar, Sachin and Dubey, Megha and Verma, Anupam and Srinag, Bangalore S and Krishnamurthy, Hanumanthappa and Barthwal, Manoj K and Dikshit, Madhu} }