Vitamin B ameliorates PM2.5-induced kidney damage by reducing endoplasmic reticulum stress and oxidative stress in pregnant mice and HK-2.

As an air pollutant, particulate matters 2.5 (PM2.5) poses a severe risk to kidney and the mechanism involves oxidative stress and endoplasmic reticulum (ER) stress. As an essential nutrient for human health, Vitamin B performs anti-inflammatory and antioxidant functions. In order to study the effect of Vitamin B on PM2.5-induced kidney damage during pregnancy, the pregnant mice were divided into the four experimental groups randomly: control group, model group, treatment group and VB group. PM2.5 was sprayed on the trachea of pregnant mice once each three days for six times from pregnancy until delivery. The model group was given 30 µL PM2.5 suspension of 3.456 µg/µL and 10 mL/(kg·d) PBS. The treatment group was given 30 µL PM2.5 suspension of 3.456 µg/µL and 10 mL/(kg·d) Vitamin B. The VB group was given 10 mL/(kg·d) Vitamin B and the control group was given the same dose of PBS. Vitamin B was composed of Vitamin B6, Vitamin B12 and folic acid, with final concentrations are 1.14, 0.02 and 0.06 mg/mL, respectively. The results showed Vitamin B ameliorated PM2.5-induced kidney damage such as improving histopathological change, decreasing expressions of Bip and Chop, increasing expressions of Nrf2, HO-1 and Nqo1. In addition, HK-2 cells were used for cell experiments and were divided into the four groups, in which the dosage of PM2.5 was 75 µg/mL for 24 h and Vitamin B was 5 µL/100 µL. The results showed Vitamin B ameliorated PM2.5-induced HK-2 damage, such as decreasing expressions of Bip, Chop, P47phox and ROS, increasing expressions of Nrf2, HO-1, Nqo1 and NO. Our findings showed Vitamin B ameliorated PM2.5-induced kidney damage by reducing ER stress and oxidative stress in pregnant mice and in HK-2.

The impact of PM2.5 on kidney.

PM2.5 poses a severe risk to kidneys, inducing kidney function decline, increasing the risk of suffering from chronic kidney diseases and promoting the occurrence and development of various renal tumors. The mechanism of PM2.5-induced renal injury may involve oxidative stress, inflammatory response, and cytotoxicity. This paper elaborated PM2.5-induced kidney damage and the corresponding possible mechanism so as to raise awareness of air pollution and reduce the damage to human body.

Mechanism of kidney injury induced by cisplatin.

Cisplatin is a common metal platinum complex. The platinum atom in the molecule is of great significance to its antitumor effect. Clinically, it can show curative effect on a variety of solid tumors. However, cisplatin has certain adverse effects in treatment, one among which is acute renal injury (AKI). Except for the nuclear DNA damage caused by cisplatin, damage of organelles, and cytoplasm also contribute to side effects. Endoplasmic reticulum stress, mitochondrial apoptosis pathway or cascade reaction caused by complement and caspase protein also play important roles in cisplatin induced renal injury. Therefore, the damage studies of organelles and cytoplasm are also necessary for exploring adverse effects of cisplatin. This paper reviews the damage of endoplasmic reticulum, mitochondria, and indirect DNA apoptosis pathways induced by cisplatin. It also explains in detail why cisplatin is easy to cause kidney damage. Deep understanding of such interactions could be helpful to exploit better drugs which would minimize kidney injury and maximize anti-tumor effects of cisplatin.