VERNONIA CINEREA (NEICHITTI KEERAI) REGENERATES PROXIMAL TUBULES IN CISPLATININDUCED RENAL DAMAGE IN MICE

Objective: The aim of the study was to evaluate whether Vernonia cinerea (VC) regenerates the proximal renal tubular cells in cisplatin-induced necrosis in male Swiss albino mice.Methods: The crude aqueous extract (CAE) of VC was fractionated from non-polar to polar using different solvents. Mice were injected a single dose of cisplatin (15 mg/kg) on day 1, which took 5 days to cause maximal renal damage. From day 6, CAE and all fractions were orally administered (200, 300, and 400 mg/kg) for 5 continuous days. On day 11, blood was collected to estimate urea and creatinine. Kidney was collected for histology and grading was done.Results: Cisplatin induced proximal renal tubular damage (grade 5) in corticomedullary junction, characterized by necrosis, proximal tubular dilatation, inflammation and vasodilation. Aqueous fraction (AF) did not show any regeneration; whereas, 400 mg/kg dose of CAE and butanol fraction (BF) showed a significant reduction (p<0.001) in proximal tubular damage (Grade 3) and 50–75% regeneration of proximal tubular epithelial cells.Conclusion: This is the first study to demonstrate the regenerative potential of Neichitti kashayam (CAE of VC) and its BF in cisplatin-induced proximal tubular damage in kidney. Further study is warranted to find out the dose regimen for complete regeneration, lead compounds, and molecular mechanism

PROTECTIVE EFFECT OF KADUKKAI MAATHIRAI (TERMINALIA CHEBULA-BASED POLYHERBAL SIDDHA FORMULATION) IN ETHANOL-INDUCED LIVER DISEASE IN RATS

Objective: The objective of this study was to evaluate the prophylactic effect of Kadukkai maathirai (KM) against ethanol-induced hepatotoxicity in rats.Methods: Four groups (n=6) of adult female Sprague–Dawley rats were used. Ethanol was administered in the dose of 45% v/v 15 mL/kg/body weight twice a day for 8 weeks in the study. The four groups were treated orally for 8 weeks with 2% gum acacia (control), ethanol (toxic control), ethanol + KM 72 mg/kg, and ethanol + KM 400 mg/kg, respectively. At the end of 8 weeks, blood was collected by a retro-orbital puncture for the estimation of liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]). The liver was dissected out for histopathology. Using one-way ANOVA and post hoc Tukey's test, the data were analyzed.Results: There was a significant (p<0.05) decrease in the serum AST and ALT level in rats treated with KM 72 mg/kg as compared to toxic control. Liver parenchyma showed near normal architecture in KM 72 mg/kg-treated group as compared to ethanol-treated group which showed extensive ballooning degeneration of hepatocytes and microvesicular steatosis.Conclusion: KM, in the dose of 72 mg/kg, which is the therapeutic dosage described in Siddha additional literature, exerted hepatoprotective effect against ethanol-induced liver damage in rats

Correction: Physiochemical characterization and cytotoxicity evaluation of mercury-based formulation for the development of anticancer therapeuticals.

[This corrects the article DOI: 10.1371/journal.pone.0195800.]

Deformities in zebrafish embryo development at 1 mg/ml concentration (a) head and tail (b) yolk sac edema and (c) pericardial edema.

<p>Deformities in zebrafish embryo development at 1 mg/ml concentration (a) head and tail (b) yolk sac edema and (c) pericardial edema.</p

XPS analysis of PK formulation.

<p>XPS analysis of PK formulation.</p

The cell viability of MCF-7.

<p>The cell viability of MCF-7.</p

Trypan blue stained MCF-7 cells after treatment with control and higher concentration.

<p>Trypan blue stained MCF-7 cells after treatment with control and higher concentration.</p