Pregnancy complications are associated with oxidative stress induced by accumulation of trophoblastic ROS in the placenta. We employed the human trophoblast HTR8/SVneo cell line to determine the effect of curcumin pre-treatment on H₂O₂-induced oxidative damage in HTR8/Sveo cells. Cells were pretreated with 2.5 or 5 μM curcumin for 24 h, and then incubated with 400 μM H₂O₂ for another 24 h. The results showed that H₂O₂ decreased the cell viability and induced excessive accumulation of reactive oxygen species (ROS) in HTR8/Sveo cells. Curcumin pre-treatment effectively protected HTR8/SVneo cells against oxidative stress-induced apoptosis via increasing Bcl-2/Bax ratio and decreasing the protein expression level of cleaved-caspase 3. Moreover, curcumin pre-treatment alleviated the excessive oxidative stress by enhancing the activity of antioxidative enzymes. The antioxidant effect of curcumin was achieved by activating Nrf2 and its downstream antioxidant proteins. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage. Taken together, our results show that curcumin could protect HTR8/SVneo cells from H₂O₂-induced oxidative stress by activating Nrf2 signaling pathway.

The aim of this study was to investigate the antioxidant effects of curcumin and bisdemethoxycurcumin in both 2,20-azobis(2-amidinopropane) dihydrochloride (AAPH)-treated erythrocytes and broiler chickens. In experiment 1, chicken erythrocytes were employed to determine the antioxidant protection against AAPH treatment. Significant differences in hemolysis, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content were observed between the control and curcuminoids-treated groups. In experiment 2, a total of 480 Arbor Acres broilers with the similar body weights were used. All of the birds were fed basal diet and basal diet with 150 mg/kg curcumin or bisdemethoxycurcumin, respectively. The results showed that curcuminoids significantly increased ADG, serum antioxidant capacity, the glutathione redox potential of small intestine, the gene expression of Nrf2, and its related antioxidant enzymes. Besides, curcumin and bisdemethoxycurcumin increased the antioxidant activities of serum, diet, and excreta while using the 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt and ferric-reducing antioxidant power methods. It was concluded that bisdemethoxycurcumin, acting like curcumin, exerted good free radical scavenging activity in erythrocytes and improved the redox status in broilers, although there were some slight differences in their efficiency of antioxidant activities.

Our previous study showed that bisdemethoxycurcumin (BUR) exerts anti-inflammatory properties in lipopolysaccharide-induced intestinal injury, and studies have revealed that NOD-like receptor superfamily, pyrin domain containing 3 (NLRP3) inflammasome activation plays a vital role in the pathogenesis of colitis. However, it is not clear whether BUR could attenuate colitis-mediated intestinal inflammation via NLRP3 inflammasome inactivation and modulate the gut microbiota dysbiosis. The results demonstrated that BUR attenuated DSS-induced body weight decrease, histopathological changes, and epithelial apoptosis. BUR significantly improved the intestinal barrier defects and abrogated DSS-induced inflammatory response. Consistently, BUR reduced the expression of NLRP3 family members, confirming its inhibitory effects on NLRP3 inflammasome activation and pyroptosis. BUR regulated microbiota dysbiosis and altered the gut microbial community. BUR supplementation enriched the relative abundance of beneficial bacteria (such as Lactobacillus and Bifidobacterium), which showed significant negative correlations with the pro-inflammatory biomarkers. Collectively, these findings illustrated that BUR could ameliorate DSS-induced colitis by improving intestinal barrier function, reducing apoptosis, inhibiting NLRP3 inflammasome activation, and regulating the gut microbiota.

This study aimed to investigate the effects of dietary dihydroartemisinin on the growth performance, meat quality, and antioxidant capacity of broiler chickens. Four-hundred one-day-old Arbor Acres male broilers were randomly assigned to five treatment groups with eight replicates and ten birds each. All broilers were fed a basal diet containing 0, 5, 10, 20 or 40 mg/kg dihydroartemisinin. The results showed that dihydroartemisinin at 10 mg/kg quadratically increased ADG, and dihydroartemisinin at 10 and 20 mg/kg quadratically increased ADFI during the days 1-21 period. Compared to the control group, dihydroartemisinin at 10 and 20 mg/kg quadratically decreased the drip loss at 24 h. Dihydroartemisinin linearly and quadratically decreased the L* value of breast muscles. Dihydroartemisinin at 20-40 mg/kg linearly and quadratically decreased the MDA concentrations at D5 and D 7 of postmortem storage. Dihydroartemisinin linearly and quadratically increased the ABTS scavenging activity at D 7 of postmortem storage. Dietary 20 mg/kg dihydroartemisinin at 21 days and 40 mg/kg dihydroartemisinin at 42 days linearly and quadratically increased serum glutathione concentrations. Dihydroartemisinin at 5-40 mg/kg linearly increased serum total superoxide dismutase activity at 42 days. Dihydroartemisinin at 10-20 mg/kg quadratically decreased serum malondialdehyde contents at 42 days. At 21 days, 20 mg/kg dihydroartemisinin quadratically increased hepatic glutathione concentrations and catalase activities. Compared to the control group, 40 mg/kg dihydroartemisinin linearly and quadratically decreased hepatic malondialdehyde contents. At 42 days, 20 mg/kg dihydroartemisinin quadratically increased catalase activities and reduced the malondialdehyde contents in liver. Dihydroartemisinin quadratically increased the hepatic mRNA expression of Nrf2. Compared to the control group, dihydroartemisinin at 10 and 20 mg/kg quadratically induced the hepatic mRNA expression of HO-1. Dihydroartemisinin at 10-40 mg/kg linearly and quadratically increased the mRNA expression of CAT in liver. These results showed that dihydroartemisinin improved growth performance, meat quality, and antioxidant capacity of broiler chickens, especially at 10 and 20 mg/kg.

This study aimed to investigate the effects of leucine with different levels on the insulin resistance in intrauterine growth restriction/retardation (IUGR) piglets. Thirty-two weaned piglets were arranged in a 2 × 2 factorial design and four treatments (n = 8) were as follow: (1) normal weaned piglets fed a basal diet (CONT), (2) IUGR weaned piglets fed a basal diet (IUGR), (3) normal weaned piglets fed a basal diet with the addition of 0.35% l-leucine (C-LEU), and (4) IUGR fed a basal diet with the addition of 0.35% l-leucine (I-LEU) for a 21-days trial. The results showed that compared to the IUGR group, the I-LEU group had higher final body weight and body weight gain, higher serum glucose concentrations, and higher serum insulin concentrations (p < 0.05). The gene expression of phosphatidylinositol 3-kinase p110 gamma, protein kinase adenosine monophosphate-activated γ 3-subunit, glycogen synthase kinase-3 alpha, and glucose transporter type 2 were increased in the I-LEU group as compared to the IUGR group (p < 0.05). It was concluded that dietary leucine supplementation restored serum glucose concentrations, increased insulin and creatinine concentrations, and enhanced protein kinase adenosine monophosphate-activated γ 3-subunit and glucose transporter type 2 expression, suggesting that leucine might play a positive role in hepatic lipid metabolism and glucose metabolism in IUGR.

The current study sought to understand the mechanism underlying skeletal muscle dysfunction brought on by intrauterine growth restriction (IUGR) and to explore the treatment benefits of applying dimethylglycine sodium salt (DMG-Na) in sow milk to newborns during the suckling period. Each of the 10 sows delivered one newborn with a normal birth weight (NBW) and one with an IUGR. Additionally, two NBW and two IUGR newborns were collected per litter of another 10 sows. The 20 NBW newborns were divided between the N (sow milk) and ND (sow milk + 0.1% DMG-Na) groups, while 20 IUGR newborns were divided between the I (sow milk) and ID (sow milk + 0.1% DMG-Na) groups. The skeletal muscle histomorphology, redox status, and levels of gene and protein expression were worse (p < 0.05) in the I group than in the N group. In addition, supplementation with DMG-Na (ND and ID groups) improved (p < 0.05) those parameters compared to the unsupplemented groups (N and I groups). Inhibited nuclear factor erythroid 2-related factor 2 (Nrf2)/sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptorγcoactivator-1α (PGC-1α) activity resulted in decreased redox status, skeletal muscle structural damage, skeletal muscle mitochondrial function impairment, and decreased performance in IUGR newborns. Supplementation of DMG-Na in sow milk activated the Nrf2/SIRT1/PGC-1α in IUGR newborns, thereby improving their skeletal muscle performance.