Pre-Clinical Research
Pre-clinical research has investigated the biological activity of Turmesac® across cellular and animal models of inflammation, oxidative stress, liver injury and abnormal cell proliferation. These studies help establish possible mechanisms of action and provide the scientific groundwork required before effects can be evaluated in well-controlled human clinical trials.
Anti-inflammatory activity in chemically induced animal models
Croton oil induced ear edema in Swiss albino mice and histamine induced paw edema in Wistar albino rats.
To evaluate whether oral Turmesac® could reduce acute inflammation produced by two chemically induced experimental models.
Animals received Turmesac® at 250 or 500 mg/kg body weight. Diclofenac sodium at 10 mg/kg was used as the reference drug. Ear edema was measured after croton oil application, while paw volume was monitored after histamine exposure.
Turmesac® reduced inflammation in a dose-dependent manner. At 500 mg/kg, it produced 58.65% inhibition of croton oil induced ear edema after two hours and 57.25% inhibition after four hours. Both tested doses also reduced histamine induced paw edema, with the higher dose showing stronger activity.
The results indicate that Turmesac® can influence acute inflammatory responses involving edema, vascular permeability and chemical mediators such as histamine. These findings remain pre-clinical and do not establish therapeutic effects in humans.
Firoz H. M., Nanjundaiah S. and Sadashiva C. T. European Journal of Biomedical and Pharmaceutical Sciences, 2020; 7(6):439-443.
Modulation of inflammatory cytokines in macrophages
Lipopolysaccharide-stimulated RAW 264.7 murine macrophage cells.
To determine whether Turmesac® could suppress inflammatory cytokine expression in activated immune cells.
RAW 264.7 cells were stimulated with lipopolysaccharide at 2 µg/ml and treated with a non-cytotoxic Turmesac® concentration of 50 µg/ml. Expression of IL-8 and IL-12 was measured by flow cytometry.
Lipopolysaccharide increased mean fluorescence intensity for IL-8 from 8.86 to 50.49 and for IL-12 from 10.41 to 68.94. Incubation with Turmesac® reduced these values to 19.63 for IL-8 and 15.79 for IL-12.
Suppression of these pro-inflammatory cytokine signals provides a cellular mechanism that may help explain the anti-inflammatory activity observed in the animal models.
Firoz H. M., Nanjundaiah S. and Sadashiva C. T. International Journal of Pharmacy and Pharmaceutical Sciences, 2020; 12(9):49-53.
Protection against paracetamol induced liver injury
Paracetamol induced hepatotoxicity in Wistar albino rats.
To assess the hepatoprotective and antioxidant effects of Turmesac® following chemically induced liver injury.
Rats received Turmesac® at 250 or 500 mg/kg daily with paracetamol at 2 g/kg. Silymarin at 50 mg/kg served as the positive control. Serum liver markers, antioxidant enzymes and liver histology were evaluated.
The 500 mg/kg dose reduced SGOT from 929 to 568 IU/L, SGPT from 829 to 546 IU/L and total bilirubin from 0.25 to 0.13 mg/dL compared with the toxic control. Turmesac® also increased glutathione, superoxide dismutase, catalase and total protein. Histological examination showed reduced tissue degeneration and improved liver architecture.
The combined biochemical and histological findings suggest that Turmesac® may protect liver tissue by attenuating oxidative stress and supporting endogenous antioxidant defences.
Sadashiva C. T., Firoz Hussain H. M. and Nanjundaiah S. European Journal of Biomedical and Pharmaceutical Sciences, 2020; 7(2):402-409.
Cellular antioxidant and hepatoprotective activity
H₂O₂-stressed HepG2 and HUH-7 human liver cell models.
To examine whether Turmesac® could reduce oxidative stress and preserve cell viability after hydrogen peroxide exposure.
HepG2 cells exposed to 200 µM H₂O₂ were treated with 50 µg/ml Turmesac®, and intracellular reactive oxygen species were measured using H2DCF-DA flow cytometry. A separate HUH-7 study tested concentrations from 25 to 400 µg/ml using an MTT viability assay.
In HepG2 cells, H₂O₂ increased mean reactive oxygen species fluorescence to 52.5, while incubation with Turmesac® reduced it to 14.43, close to the untreated control value of 7.72. In HUH-7 cells, Turmesac® produced concentration-dependent protection against H₂O₂-induced toxicity.
Reduced intracellular oxidative burden in human-derived liver cells supports the antioxidant and hepatoprotective activity observed in the animal model.
Cytotoxicity and apoptosis in cancer cell models
HeLa cervical adenocarcinoma and MCF-7 breast adenocarcinoma cells.
To investigate cytotoxicity, apoptosis induction and cell-cycle effects.
Cell viability was measured by MTT assay. HeLa cells were further evaluated by Annexin V and propidium iodide flow cytometry following exposure at the calculated IC₅₀ concentration.
Turmesac® produced an IC₅₀ of 115.12 µg/ml in HeLa cells and an IC₅₀ of 163.19 µg/ml in MCF-7 cells. In HeLa cells, total apoptosis reached 83.93%, compared with 44.19% for camptothecin. Changes were also observed in the sub-G0/G1, G0/G1, S and G2/M cell-cycle populations.
Apoptosis induction and cell-cycle modulation in selected cancer cell lines support further investigation of Turmesac® in cellular models of abnormal proliferation. These are laboratory observations only.
Summary of pre-clinical findings
- Reduced experimentally induced edema and inflammatory cytokine expression
- Suppressed reactive oxygen species and supported antioxidant enzyme activity
- Improved biochemical markers and tissue architecture in a liver injury model
- Demonstrated cytotoxicity, apoptosis induction and cell-cycle modulation in selected cancer cell lines
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Complete publications, charts and histopathology images are available to qualified partners on request.