Biotechnology

Purpose: Ulcerative colitis (UC) is associated with tainted neutrophil infiltration, deregulated proinflammatory mediators, characterized by severe oxidative stress of the intestine. In the present study,
an effort was made to evaluate the effect of methanolic fractions of Eupatorium triplinerve (E. triplinerve)
(ET) on acetic acid induced ulcerative colitis in male adult mice.
Methods: Colitis in mice was induced with 3.0% acetic acid (v/v) in saline via rectal route. Pre-intervention
with E. triplinerve extract (100 mg and 200 mg kg−1 body weight, oral) and reference drug ranitidine
(50 mg kg−1 body weight used as reference, oral) 4 days before induction of colitis and was extended
up to 8 days.
Results: The phase of inflammation before E. triplinerve extract pre-treatment significantly showed
attenuated macroscopic damage, argyrophilic nuclear organization regions (AgNORs) count and histological changes. Similarly, extract also effectively detracts the activity of both Myeloperoxidase
(MPO) and Malondialdehyde (MDA) levels by enhancing the cellular antioxidant enzyme levels
(Glutathione-s-transferase [GST], Glutathione peroxidise [GPx] and Catalase [CAT]) at the site of
ulceration.
Conclusions: The E. triplinerve based therapy resolved that some constituents in extract have an antiulcer
effect against UC at colon specific area through its inviolable radical scavenging activity.

New strategies for the prevention of colon cancer persists a crucial need. However, resistance to current
chemopreventive drugs is relatively prevalent in colon carcinogenesis. For this intent, a chemopreventive
study was acquitted to elucidate the probable effect of taxifolin (TAX) against 1,2-dimethylhydrazine
(DMH) induced colon carcinogenesis in mice and to evaluate its efficacy with 5-fluorouracil (5-FU) drug
control. Swiss Albino mice were intended for colon carcinogenesis received subcutaneous injections of
DMH (20 mg/kg bw., sc) once a week for 15 weeks and were treated with TAX (4 g/kg bw, op) and 5-FU
drug control (10 mg/kg bw., op) for the entire study period. Our results unveil that mice administered with
TAX significantly modulates DMH induced histological alterations (ACF, AgNORs, and mucin depletion).
Moreover, TAX treatment also inhibits DMH mediated oxidative damage by diminishing tissue lipid
peroxidation (MDA, MPO and CD) accompanied by enhanced activities of enhanced activities of free
radical metabolizing enzymes (SOD, CAT, GPx, GR, GSH, vitamin A, C and E). Apoptotic and proliferating
cell nuclear antigen (PCNA) findings also revealed that treatment with TAX substantially regulates cell
proliferation through the increased extent of DNA fragmentation. The incidence of colon cancer in TAX
treated mice was significantly reduced when compared to that of 5-FU control. Our findings concluded
that taxifolin act as an effective chemopreventive agent against colon carcinogenesis by its virtue of
antioxidant mediated apoptosis and anti-proliferative activities.

Breast cancer is one of the leading cancer types in women across the world. Computer aided drug designing have been widely applied for drug development and discovery of potential drug molecule of many over expressed proteins induced in breast cancer. In the present study HIF-1a is targeted as receptor and peptides targeted as ligands through protein-protein interaction. A total of 352 peptides were docked with the predicted binding sites of HIF-1a and found that 9 peptides exhibited encouraging binding and docking energy. The maximum docking interactions score of À38.15 kJ/mol was observed between a peptide FALALKA and HIF-1a. By analyzing docking study results, amino acid Aspartic acid (Asp 187) play a crucial role forming H-bond and hydrophobic interactions with all the 9 peptides. Taken together, the results of present findings throws light on the design of novel HIF-1a antagonist peptides and aspartic acid could considered during its design for implying its action as a best antagonist against the HIF-1a receptor.