Table 1.
Polyphenolic compounds identified in the ethanol leaf extract of G. procumbens.
Fig 1.
HPLC chromatogram of the ethanolic extract of Gynura procumbens [corresponding peaks: 1, gallic acid; 2, ellagic acid; 3, rutin hydrate; 4, quercetin hydrate; 5, kaempferol].
Fig 2.
Pseudo-ternary phase diagram of GLE microemulsions in water.
KP, Kolliphor® P188 (Surfactant); MCT, medium chain triglyceride (oil); PG, propylene glycol (Co-surfactant); and GLE, Gynura procumbens Extract. ● (filled area), fine emulsion region; ▽, coarse emulsion region; and ○, poor or not emulsified.
Fig 3.
Micelle forming potency of GLE samples dispersed in water.
(A) DLS analysis determined the emulsion size distribution of SMEDDS-GLE spread in distilled water: The solid line represents the micelle size distribution at 0 min after dispersion, and the dotted line represents the micelle size distribution at 3 h after dispersion. (B) TEM image of SMEDDS-GLE dispersed in distilled water. Bar represents 200 nm.
Fig 4.
Dissolution/dispersion tests of GLE samples (A) Dissolution/dispersion tests in distilled water; (B) Dissolution/dispersion tests under acidic conditions (0.1 N HCl, pH 1.2).
●, GLE and △, SMEDDS-GLE. Each bar represents the mean ± S.D. of 3 independent experiments.
Fig 5.
ATR-FTIR spectroscopic analysis of GLE samples in the spectral region from (A) 4,000–600 cm–1 and (B) 1,800–1,300 cm–1.
(I) SMEDDS-GLE, (II) PG, (III) MCT, (IV) Kolliphor® P188, and (V) GLE.
Fig 6.
Effect of GLE samples on hepatic markers in the rat liver: (A) Alanine aminotransferase (ALT), (B) Aspartate Amino Transferase (AST), and (C) Alkaline Phosphatase (ALP) levels.
The data were expressed as Mean ± S.E.; n = 6, where n is the number of determinations. * , P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; with respect to cisplatin-treated rats; ##, P < 0.01, GLE vs. SMEDDS-GLE. Data represent mean ± S.E. of 6 experiments.
Fig 7.
Histopathological examination of the effect GLE samples on cisplatin-treated liver using hematoxylin and eosin staining.
(A) Rats treated with saline, (B) cisplatin-treated rats, (C) rats treated with GLE, (D) cisplatin-treated rats with silymarin (E) cisplatin-treated rats with GLE, and (F) cisplatin-treated rats with SMEDDS-GLE. All the rat livers were sectioned at 5 μm using microtome, and stained with hematoxylin and eosin. The stained sections were studied under light microscope at a magnification of × 40. Each bar represents 100 µm. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; with respect to cisplatin-treated rats.
Fig 8.
Nephrotoxic potential in a rat nephropathy model induced by cisplatin.
(A) Plasma creatinine and (B) BUN levels in rats with orally dosed GLE and SMEDDS-GLE. **, P < 0.01; ****, P < 0.0001; with respect to cisplatin-treated rats; #, P < 0.05, GLE vs. SMEDDS-GLE. Data represent mean ± S.E. of 6 experiments.
Fig 9.
Histopathological examination of the effect GLE samples on cisplatin-treated kidney using hematoxylin and eosin staining. (A) Rats treated with saline, (B) cisplatin-treated rats, (C) rats treated with GLE, (D) cisplatin-treated rats with silymarin (E) cisplatin-treated rats with GLE, and (F) cisplatin-treated rats with SMEDDS-GLE.
All the rat kidneys were sectioned at 5 μm using a microtome, and stained with hematoxylin and eosin. The stained sections were studied under a light microscope at a magnification of × 40. Each bar represents 100 µm. * , P < 0.05; ***, P < 0.001; ****, P < 0.0001; with respect to cisplatin-treated rats.