Unani Formulation Habb-e-Suranjan: A Treasure of Biological Activities.

Habb-e-Suranjan (HES), an Unani formulation, has been studied for its anti-inflammatory properties in both in vitro and in vivo experiments. HES is recommended for arthritis, gout, and joint pain. The current endeavor is an attempt to put it to the test and verify its efficacy scientifically. It was tested for DPPH, hydroxyl, and nitric oxide scavenging activities. It was shown that HES had the greatest TAC and FRAC values when compared to catechin and ascorbic acid. HES exhibited DPPH and hydroxyl radical scavenging activity that was dose-dependent. Incubation of sodium nitroprusside solutions in PBS at 25°C for 150 min resulted in the production of nitric oxide. Nitric oxide production was effectively decreased by HES. Anti-inflammatory medications boosted the migration of PMN cells toward the chemoattractant FMLP in an agarose experiment of PMN chemotaxis. In carrageenan-induced rat paw edema, in the HES-treated group, paw thickness was 3.021 ± 0.084 at t = 0, but it showed an increase in paw inflammation after one hour, i.e., 3.195 ± 0.082 cm which again showed a decrease in paw thickness up to 4th hour, i.e., 3.018 ± 0.078, 2.98 ± 0.032, and 2.684 ± 0.061 at t = 2, 3, and 4, respectively. It showed again getting back to the normal thickness of paw at t = 24 hrs, i.e., 3.029 ± 0.118 cm. It is concluded that the formulation is potent enough and can be used effectively for the treatment of inflammation and associated health issues. Moreover, there is much scope to evaluate its effectiveness using different in vitro and in vivo models.

DT-13 inhibits breast cancer cell migration via non-muscle myosin II-A regulation in tumor microenvironment synchronized adaptations.

BACKGROUND: Tumor metastasis is a terrifying characteristic of cancer. Numerous studies have been conducted to overcome metastasis by targeting tumor microenvironment (TME). However, due to complexity of tumor microenvironment, it remained difficult for accurate targeting. Dwarf-lillytruf tuber monomer-13 (DT-13) possess good potential against TME. OBJECTIVE: As TME is supportive for tumor metastasis, alternatively it is a challenging for therapeutic intervention. In our present study, we explored molecular mechanism through which TME induced cell migration and how DT-13 interferes in this mechanism. METHODS: We used a novel model of co-culture system which is eventually developed in our lab. Tumor cells were co-cultured with hypoxia induced cancer-associated fibroblasts (CAF) or with chemically induced cancer-associated adipocytes (CAA). The effect of hypoxia in conditioned medium for CAF was assessed through expression of α-SMA and HIF by western blotting while oil red staining was done to assess the successful chemical induction for adipocytes (CAA), the effect of TME through conditioned medium on cell migration was analyzed by trans-well cell migration, and cell motility (wound healing) analyses. The expression changes in cellular proteins were assessed through western blotting and immunofluorescent studies. RESULTS AND CONCLUSION: Our results showed that tumor microenvironment has a direct role in promoting breast cancer cell migration by stromal cells; moreover, we found that DT-13 restricts this TME regulated cell migration via targeting stromal cells in vitro. Additionally we also found that DT-13 targets NMII-A for its effect on breast cancer cell migration for the regulation of stromal cells in TME.

In-silico Studies Show Potent Inhibition of HIV-1 Reverse Transcriptase Activity by a Herbal Drug.

Acquired immunodeficiency syndrome (AIDS) is a life threatening disease of the human immune system caused by human immunodeficiency virus (HIV). Effective inhibition of reverse transcriptase activity is a prominent, clinically viable approach for the treatment of AIDS. Few non-nucleoside reverse transcriptase inhibitors (NNRTIs) have been approved by the United States Food and Drug Administration (US FDA) as drugs for AIDS. In order to enhance therapeutic options against AIDS we examined novel herbal compounds of 4-thiazolidinone and its derivatives that are known to have remarkable antiviral potency. Our molecular docking and simulation experiments have identified one such herbal molecule known as (5E)-3-(2-aminoethyl)-5-benzylidene-1, 3-thiazolidine-2,4-dione that may bind HIV-1RT with high affinity to cause noncompetitive inhibition. Results are also compared with other US FDA approved drugs. Long de novo simulations and docking study suggest that the ligand (5E)-3-(2-aminoethyl)-5-benzylidene-1, 3-thiazolidine-2,4-dione (CID: 1656714) has strong binding interactions with Asp113, Asp110, Asp185 and Asp186 amino acids, all of which belong to one or the other catalytic pockets of HIV-1RT. It is expected that these interactions could be critical in the inhibitory activity of the HIV-1RT. Therefore, this study provides an evidence for consideration of (5E)-3-(2-aminoethyl)-5-benzylidene-1, 3-thiazolidine-2,4-dione as a valuable natural molecule in the treatment and prevention of HIV-associated disorders.

Structural, functional and therapeutic biology of survivin.

Survivin is a unique member of the inhibitor of apoptosis (IAP) protein family that interferes with post-mitochondrial events including activation of caspases. Survivin regulates cell cycle also. It is expressed in most of the human tumors, but it is barely detectable in the terminally differentiated normal cells/tissues. Molecular mechanisms of regulation of survivin in cancer are not clearly understood. Nevertheless, the functional loss of wild type p53 is often associated with upregulation of survivin. Tumors that over-express survivin generally bear a poor prognosis and are associated with resistance to therapy. The differential expression of survivin in cancer versus normal tissues makes it a useful tool in cancer diagnosis and a promising therapeutic target. A growing body of literature suggests nuclear expression of survivin as a good prognostic marker. Disruption of the survivin induction pathway has resulted in an increase in apoptosis and inhibition of tumor growth. Regular therapies, such as, radiotherapy in combination with anticancer drugs in clinical practice may yield promising results.