Baicalin Ameliorates Lung Injury in Rats by Inhibiting NLRP3 Inflammasome Activation via NF-[Formula: see text]B Signaling Pathway.

Hemorrhagic shock (HS) is defined as a reduction in tissue oxygenation and organ dysfunction due to severe blood loss. Lung injury is a frequent complication of HS. Baicalin, isolated from Radix Scutellariae, has been reported to profile the antitumor, anti-oxidative, anti-inflammatory, and antibacterial roles in various pathological processes. Nevertheless, the effects of baicalin on HS-induced lung injury are unclear. This study aims to examine the therapeutic effects of baicalin on lung injury. We first established the lung injury rat models by withdrawing blood in the femoral artery followed by resuscitation. A pathological analysis showed that HS-administrated rats presented severe capillary leakage and pulmonary edema, while baicalin therapy alleviated the symptoms. Baicalin therapy reduced the number of macrophages and neutrophils in bronchoalveolar lavage fluid and decreased the expression and activity of myeloperoxidase (neutrophile infiltration marker) in the lung tissues of HS rats, indicating that baicalin alleviated HS-induced infiltration of inflammatory cells. The secretion of inflammatory cytokines, including interleukin (IL)-1[Formula: see text], IL-6, IL-18, and tumor necrosis factor [Formula: see text] (TNF-[Formula: see text]), as well as the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) inflammasome, were inhibited by baicalin administration. Furthermore, we found that the NF-[Formula: see text]B pathway, a canonical pro-inflammatory pathway, was also blocked after treatment with baicalin in HS-evoked rats, as indicated by the decreased expression of p65 and p65 phosphorylation in the lung tissues. In summary, we infer that baicalin may exert a protective role in HS-induced lung injury by suppressing the activation of NLRP3 inflammasome via the NF-[Formula: see text]B pathway.

Expressions and related mechanisms of miR-212 and KLF4 in rats with acute kidney injury.

Acute kidney injury (AKI) occurs in 30%-70% of critically ill patients. Multiple organ failure (MOF), which is most often secondary to hypotension and septicemia, is a global public health problem. The prognosis of patients is poor. Currently, there is no specific therapeutic method. Finding new therapeutic targets is significant to improve the prognosis of AKI patients. This study explores expressions and related mechanisms of miR-212 and Kruppel-like factor 4 (KLF4) in rats with AKI. Sixty Wistar rats were randomly divided into 6 groups: Control group, sham operation group, model group, miR-212-agomir group, miR-212-antagomir group, miR-212-agomir+APTO-253 (joint group), n = 10. The expressions of miR-212, KLF4, inflammatory factors [tumor necrosis factor α (TNF-α), interleukin 6 (IL-6)], oxidative stress factors [superoxide dismutase (SOD), malondialdehyde (MDA)], and apoptosis-related proteins (bax, bcl-2) in renal tissue of rats were detected, and the relationship between miR-212 and KLF4 and the severity of AKI in rats were analyzed. The expression level of miR-212 increased (P < 0.05) and the expression level of KLF4 decreased (P < 0.05) in renal tissue of rats with AKI. miR-212 was negatively correlated with KLF4 expression (P < 0.05). MiR-212 was positively correlated with expressions of TNF-α, IL-6, MDA, and bax (P < 0.05), negatively correlated with expressions of SOD and bcl-2 (P < 0.05), KLF4 was negatively correlated with expressions of TNF-α, IL-6, MDA and bax (P < 0.05), and positively correlated with expressions of SOD and bcl-2 (P < 0.05). MiR-212 mimics can inhibit the luciferase activity of Wt-KLF4 (P < 0.05), and miR-212 inhibitor can promote the luciferase activity of Wt-KLF4 (P < 0.05). Down-regulation of miR-212 plays a protective role by targeting up-regulation of KLF4 to inhibit renal tissue inflammation, oxidative stress, and apoptosis in rats with AKI, which may be a potential target for clinical treatment of AKI in the future.