PMC

FTIR spectra of
(a) Desmodium adscendens leaf extract, (b) Synthesised AgNPs

Activity of serum enzymes on the administration of Desmodium adscendens extract to rats for 6 weeks: (A) aspartate aminotransferase (AST), (B) alanine aminotransferase (ALT), (C) γ-glutamyl transferase (GGT). *P < .01.

Liver microsomal content and CYP activities following subchronic administration of Desmodium adscendens: (A) microsomal protein concentration, (B) paranitrophenol activity for CYP2E, (C) ethoxyresorufin-O-deethylase (EROD) activity for CYP1A1/1A2, (D) pentoxyresorufin-O-deethylase (PROD) activity for CYP2B1/2B2. *P < .01; ** P < .001.

Serum biomarker levels following subchronic administration of Desmodium adscendens: (A) creatinine concentration, (B) protein concentration, (C) total bilirubin, (D) direct bilirubin, (E) blood urea nitrogen (BUN). All statistical significance was calculated using the 2-sided t test with unequal variance. **P < .001.

The ROS levels were measured by flow cytometry. The fluorescence intensity was expressed as decimal logarithm versus the cell number. (a) and (b) are the controls corresponding to the level of intracellular ROS without and with oxidative stress, respectively. (c) is the pretreated granulocytes corresponding to ROS level in these cells incubated in the presence of Desmodium adscendens extract at 25 mg/mL then subjected to the oxidative stress.

Protective effects of Desmodium adscendens (DA) extract against oxidative stress on LLC-PK1 cell line. Cell viability of LLC-PK1 cell line was measured by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Oxidative stress was induced high glucose (30 mM) and incubated for 24 h without or with DA extract 1, 10 or 100 mg/ml). Data are represented as mean ± standard error mean of six determinations. *P < 0.05 from control

Examples of compounds isolated from D. adscendens

(a) MWE, HPLC chromatogram at 280 nm of leaves of D. adscendens 3: catechin; 6: quercetrin glucosyl; 7: quercetrin dihydrat; 8: cinnamic acid. (b) MWE, HPLC chromatogram at 320 nm of leaves of D. adscendens 4: chlorogenic acid; 5: quercetrin glycosyl; 6: quercetrin dihydrat; 7: cinnamic acid; 8: cinnamic acid.

Morphological changes observed under light microscopy. Magnification ×10. HepG2 (1) and LLC PK1 (2), (a) dimethyl sulfoxide, (b) control, (c) 1 mg/ml desmodium extract, (d) 10 mg/ml desmodium extract, (e) 100 mg/ml desmodium extract, (f) triton ×100

(a) WE, HPLC chromatogram at 280 nm of the leaves of D. adscendens 1: gallic acid; 2: protocatechuic acid; 4: rutin; 5: quercetrin glucosyl; 6: quercetrin dihydrat; 7: cinnamic acid. (b) WE, HPLC chromatogram at 320 nm of the leaves of D. adscendens 3: Catechin; 6: quercetrin glucosyl; 7: quercetrin dihydrat; 8: cinnamic acid.

Effect of Desmodium adscendens (DA) extract on cells growth. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay, (a) Cell viability of HepG2 cell line, (b) Cell viability of LLC PK1 cell line incubated for 24 h without or with DA extract 1, 10 or 100 mg/ml), dimethyl sulfoxide and triton were used as negative and positive controls respectively. Data are represented as mean ± standard error mean of six determinations. *P < 0.05 versus control

Effect of Desmodium adscendens (DA) on cell injury assessed by the lactate dehydrogenase (LDH) release, (a) LDH release of HepG2 cell line, (b) LDH release of LLC PK1 cell line incubated for 24 h without or with DA extract 1, 10 or 100 mg/ml), dimethyl sulfoxide and triton were used as negative and positive controls, respectively. Data are represented as mean ± standard error mean of six determinations. *P < 0.05 versus control

UV–Vis monitored bioreduction of Ag⁺ (0.5 mM AgNO₃) to Ag⁰ over a period of 120 h, on
(a) Gauze, (b) Plaster, (c) Antibacterial plaster using D. adscendens plant extract; FTIR monitored bioreduction of Ag⁺ (0.5 mM AgNO₃) to Ag⁰, on (d) Gauze, (e) Plaster, (f) Antibacterial plaster

UV–visible spectra of D. adscendens plant extract and SPR peaks when the extract is treated with different concentrations of AgNO₃ (0.5, 1.0, and 1.5 mM) after 12 h

Phenolic compounds of leaves of D. adscendens. TPC: Total phenolic compounds; TFC: Total flavonoid Compounds; TAC: Total anthocyanin compounds; CT: Condensed tannins; dw: dry weight; GAE: Gallic Acid Equivalent; CE: Catechin Equivalent; CgE: Cyaniding-3-glycoside Equivalent.

SEM images of
(a) Plain gauze; AgNPs on gauze synthesised from AgNO₃ solutions of (b) 0.5 mM, (c) 1 mM, (d) 1.5 mM with D. adscendens extract; (e) Plaster; AgNPs on plaster synthesised from AgNO₃ solutions of (f) 0.5 mM, (g) 1 mM, (h) 1.5 mM; (i) antibacterial plaster; AgNPs on antibacterial plaster synthesised from AgNO₃ solutions of (j) 0.5 mM, (k) 1 mM, and (l) 1.5 mM with D. adscendens extract. [Magnification of (a), (e) and (i) – 50 μm; magnification of all other photos – 500 nm]

Role of D. adcendens in prevention of diseases caused by free radicals. Generation of ROS is initiated by respiratory burst, which is set off by various physiological and environmental factors. The fabrication of an assortment of ROS from the molecular O₂, carried by different enzymes such as MPO (myloperoxidase), NADPH oxidase, and SOD (superoxide dismutase), leads to diverse cellular phenomena, namely, damage of DNA-repair proteins and caspases, lipid peroxydation, and DNA damage followed by mutation and NF-κB activation. All these phenomena give rise to wide range of diseases. D. adscendens leaves extract inhibits the generations of the free radicals by scavenging both the mother and the daughter products and also by inducing the increase of SOD, CAT, GST, and GSH, resulting in the obstruction of various disease formation.

Concentration-response curve for reduction of ROS generated by exogenous H₂O₂. R (%) ROS exo H₂O₂, reduction (%) of ROS generated by exogenous H₂O₂; CCE: Concentration of extract.

XRD spectra of untreated
(a) Gauze, (c) Plaster, (e) Antibacterial plaster; XRD spectra of (b) Gauze, (d) Plaster, (f) Antibacterial plaster treated with 0.5 mM AgNO₃ and plant extract to form immobilised capped AgNPs

AgNPs at different concentrations of Ag ions
(a) TEM image at 0.5 mM, (b) TEM image at 1.0 mM, (c) TEM image at 1.5 mM, (d) size distribution at 0.5 mM, (e) size distribution at 1.0 mM, (f) size distribution at 1.5 mM