NaCl is the main component of freshwater salinization. High NaCl concentration in drinking water can cause pulmonary hypertension syndrome (PHS) and kidney damage in broilers. To explore the effect of NaCl in drinking water on broilers’ kidneys, this study divided 80 chickens into four groups. With the control group fed with pure water, broiler chickens were fed with fresh water (FW, NaCl 1 g/L), low salt–contaminated water (L-SCW, NaCl 2.5 g/L), and high salt–contaminated water (H-SCW, NaCl 5 g/L). The results show that ascites heart index (AHI) and hematocrit (HCT) of broilers increase in L-SCW and H-SCW, the serum blood urea nitrogen and creatinine of broilers increase significantly, the kidney index increases, the kidney sections show vacuolar degeneration and fibrotic degeneration, and the TUNEL results show that the kidneys possess obvious apoptosis. In addition, the detection of RAAS-related genes (AGT gene in the liver, REN in the kidney, ACE in the lung) demonstrates that after using salt-contaminated water, the transcription levels of AGT, REN, and ACE rise significantly, and the concentration of angiotensin II (Ang II) also increases significantly. In order to verify the effect of Ang II on broiler kidneys, this research used exogenous Ang II to treat chicken embryonic kidney (CEK) cells. The results show that the cell activity of CEK decreased with the increase of the concentration of exogenous Ang II. Meanwhile, the flow cytometry assay shows that Ang II could promote the apoptosis of CEK cells. These results indicate that the salt-contaminated water can aggravate PHS and cause kidney damage. The mechanism may be related to the increase of Ang II.

Solid tumors are fairly common and face many clinical difficulties since they are hardly surgically resectable and broadly do not respond to radiation and chemotherapy. The current study aimed to fabricate ginsenoside Rg3 nanoparticles (Rg3-NPs) and evaluate their antitumor effect against Ehrlich solid tumors (EST) in mice. Rg3-NPs were fabricated using whey protein isolates (WPI), maltodextrin (MD), and gum Arabic (GA). EST was developed by the injection of mice with Ehrlich ascites cells (2.5 × 10⁶). The mice were divided into a control group, EST group, and the EST groups that were treated orally 2 weeks for with normal Rg3 (3 mg/kg b.w.), Rg3-NPs at a low dose (3 mg/kg b.w.), and Rg3-NPs at a high dose (6 mg/kg b.w.). Serum and solid tumors were collected for different assays. The results revealed that synthesized Rg3-NPs showed a spherical shape with an average particle size of 20 nm and zeta potential of -5.58 mV. The in vivo study revealed that EST mice showed a significant increase in AFP, Casp3, TNF-α, MMP-9, VEGF, MDA, and DNA damage accompanied by a significant decrease in SOD and GPx. Treatment with Rg3 or Rg3-NPs decreased the tumor weight and size and induced a significant improvement in all the biochemical parameters. Rg3-NPs were more effective than Rg3, and the improvement was dose-dependent. It could be concluded that fabrication of Rg3-NPs enhanced the protective effect against EST development which may be due to the synergistic effect of Rg3 and MD, GA, and WPI.

Vitamin B17 (VB17), also known as amygdalin and laetrile, is a type of carbohydrate occurring naturally in many plants, such as apricot kernels which have obtained a great interest in cancer therapy. This study aimed to investigate the hepatic protective potential of VB17 against Ehrlich ascites carcinoma (EAC)–bearing mice-induced liver injury, DNA damage, apoptotic P53, and PCNA alterations. A total of 100 female mice were divided into 5 groups (1st group, control group; 2nd group, VB17 group; 3rd group, EAC group; 4th group, pre-treated EAC with VB17; 5th group, co-treated EAC with VB17). Results showed that the presence of VB17 in pre-treated and co-treated groups lead to decreased DNA damage, microsomal protein, NADPH cytochrome c reductase, alpha-fetoprotein (AFP), AST, ALT, and ALP while showed increased cytochrome b5, cytochrome P450 amidopyrine N-demethylase, and aniline 4-hydroxylase compared with the EAC group. Many histopathological changes were observed in liver sections in EAC as moderate fibrosis and marked diffuse necrosis of hepatic tissue, marked inflammatory cells, and congested blood sinusoids. On the other hand, there was a moderate degree of improvement in hepatocytes in liver sections in pre-treated VB17+EAC, while a mild degree of improvement in hepatocytes, moderate cellular infiltrations, and moderate cytoplasmic vacuolization of hepatocytes in liver sections in co-treated EAC+VB17. In addition, there was a depletion in hepatic P53 and PCNA protein expression compared with the EAC group. It could be concluded that VB17 has a potential hepatoprotective effect against EAC cell–induced liver toxicity.