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. 2016 Dec 25:22:5109-5115.
doi: 10.12659/msm.899061.

Baicalin Inhibits Renal Cell Apoptosis and Protects Against Acute Kidney Injury in Pediatric Sepsis

Yanping Zhu  1 , Yanxia Fu  2 , Hairong Lin  3
Affiliations

Baicalin Inhibits Renal Cell Apoptosis and Protects Against Acute Kidney Injury in Pediatric Sepsis

Yanping Zhu et al. Med Sci Monit. .

Abstract

BACKGROUND Pediatric sepsis has high morbidity in children, may lead to acute kidney injury (AKI), and further aggravate the disease. Baicalin is a kind of flavonoid in Scutellaria baicalensis Georgi and has been reported to protect against several diseases, but its roles in septic AKI remain unclear. This study aimed to uncover the effects of baicalin in AKI during pediatric sepsis. MATERIAL AND METHODS Blood urea nitrogen (BUN) and serum creatinine (Cr) levels were detected in 50 pediatric patients, who underwent basic therapy with or without baicalin adjunctive therapy. Mouse sepsis models were constructed by cecal ligation and puncture (CLP) and treated with baicalin intragastrically, after which BUN and Cr examination, TUNEL apoptosis assay, and expression analyses of BAX and BCL2 were performed. RESULTS Baicalin adjunctive therapy significantly decreased BUN and Cr levels in pediatric sepsis patients (P<0.05). CLP led to elevated BUN and Cr levels in the mouse model (P<0.01), indicating kidney injury accompanied by sepsis. Baicalin decreased BUN and Cr levels (P<0.05), and reduced the apoptotic cell percent in the renal tissue (P<0.05) of the CLP model. It inhibited BAX and promoted BCL2 in the renal tissue, which was consistent with cell apoptosis changes. CONCLUSIONS Baicalin is capable of suppressing renal cell apoptosis and protecting against AKI in pediatric sepsis. This study provides a potential adjunctive therapy for treating AKI in pediatric sepsis, and further research is necessary to reveal its deeper mechanisms.

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Figures

Figure 1
Figure 1
Baicalin improves renal functions during pediatric sepsis. Altogether, 50 pediatric patients were analyzed. Patients (n=25) in the control group received only basic therapies and patients (n=25) in the baicalin group received basic therapies plus adjunctive baicalin oral treatment for 15 days. Blood urea nitrogen (BUN) and serum creatinine (Cr) levels were detected before and after treatment to reflect renal function changes, as shown in (A) and (B), respectively. P values are indicated for each comparison.
Figure 2
Figure 2
Baicalin improves renal functions in the cecal ligation and puncture (CLP)-induced mouse sepsis model. Altogether, 30 mice were analyzed. The sham group (n=10) went through all the surgical procedures except CLP. The CLP group (n=10) went through CLP to induce sepsis. The CLP + baicalin group (n=10) received baicalin treatment intragastrically after CLP. Blood urea nitrogen (BUN) and serum creatinine (Cr) levels were detected after 6 days, as shown in (A) and (B), respectively. P values are indicated for each comparison.
Figure 3
Figure 3
Baicalin inhibits renal cell apoptosis in the cecal ligation and puncture (CLP)-induced mouse sepsis model. (A) TUNEL assay was performed to assess cell apoptosis in the renal tissue of the 3 mouse groups. Apoptotic cells were dyed brown. Bar indicates 25 μm. (B) Average percent of apoptotic cells in the 3 mouse groups. P values are indicated for each comparison.
Figure 4
Figure 4
Baicalin regulates BAX and BCL2 expression in the cecal ligation and punctures (CLP)-induced mouse sepsis model. (A) qRT-PCR showing the expression of BCL2-associated X protein (Bax) mRNA in the 3 mouse groups. (B) qRT-PCR showing the expression of B-cell CLL/lymphoma 2 (Bcl2) mRNA in the 3 mouse groups. P values are indicated for each comparison. (C) Western blot analysis showing the protein levels of BAX and BCL2 in the 3 mouse groups. GAPDH is an internal control.
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