Dietary hawthorn-leaves flavonoids improves ovarian function and liver lipid metabolism in aged breeder hens.

Hawthorn-leaves flavonoids (HF), extracted from hawthorn leaves, were reported to exert antioxidant, anti-inflammatory and hypolipidemic properties. The aim of our study was to investigate the effects of dietary HF on the reproduction performance and liver lipid metabolism of aged breeder hens. A total of 270 aged Qiling breeder hens (60-wk-old) were randomly divided into 3 treatments: 1) basic corn-soybean diet (CON); 2) basic corn-soybean diet supplemented with 30 mg/kg HF (LHF); 3) basic corn-soybean diet supplemented with 60 mg/kg HF (HHF). The results showed that supplemented HF significantly improved the egg-laying rate and hatching rate of aged breeder hens (P < 0.05). HF treatment reduced the serum TG, T-CHO and L-LDL levels (P < 0.05), and upregulated the mRNA expressions of ESR1, ESR2, VTGⅡ, ApoB, and ApoVI in the liver (P < 0.05). Serum estrogen levels in HF treated groups were elevated compared with the CON group (P < 0.05). In the HHF group, the number of the primordial follicles was higher in comparison with the CON group (P < 0.05). Furthermore, dietary supplementation with HF improved the activity of antioxidant enzymes (T-AOC, GSH-Pχ) (P < 0.05), following with the reversed ovarian apoptosis and morphological damage. In addition, 60 mg/kg dietary HF upregulated the protein expression of PCNA and Nrf2 in the ovary (P < 0.05). In summary, dietary supplementation with HF could improve the reproduction performance through regulating liver lipid metabolism and improving ovarian function in aged breeder hens.

Hawthorne leaf flavonoids prevent oxidative stress injury of renal tissues in rats with diabetic kidney disease by regulating the p38 MAPK signaling pathway.

Objectives: Diabetic kidney disease (DKD) is the primary microvascular complication of diabetes. The incidence rate of DKD has increased worldwide, and DKD has become one of the most important causes of end-stage renal disease. In this study, we aimed to investigate the effects of hawthorn leaf flavonoids (HLF) on oxidative stress injury of renal tissue in DKD rats, and elucidate their mechanism(s) of action. Methods: A total of 35 male Sprague Dawley rats were randomly divided into the control group (CON group) and model group. Rats in the model group were fed a diet containing high sugar and fat and were injected with streptozotocin (STZ) into the abdominal cavity to induce diabetes. Diabetic rats that showed >50% increase in 24 h urine volume and >30 mg of 24 h urine protein excretion were selected as DKD model rats. After DKD models were successfully established, model rats were randomly divided into the diabetic kidney disease group (DKD group), irbesartan group (IRB group), and hawthorn leaf flavonoids group (HLF group). All rats were sacrificed at 12 weeks (w) after DKD models were established. Body weight and 24 h urinary protein levels were measured at 4 w, 8 w, and 12 w, respectively. Blood was collected to measure the levels of urea nitrogen, creatinine, triglyceride, nitric oxide, malondialdehyde, and superoxide dismutase. Pathologic changes in renal tissue were examined by hematoxylin and eosin (H&E) and Masson staining. Protein expression of p38MAPK and p-p38MAPK was determined by immunohistochemistry. Results: Our data showed that HLFs improved the general condition and body weight, and reduced the levels of urinary protein in model rats. Rats in the DKD group had more serious pathological damage in the kidney when compared to rats in the HLFs group. In addition, rats in the HLF group had significantly lower levels of urea nitrogen, creatinine, triglyceride, and malondialdehyde, and significantly higher levels of nitric oxide and superoxide dismutase than rats in the DKD group. Furthermore, p38MAPK and p-p38MAPK protein levels were significantly higher in rats in the DKD group compared to rats in the HLF group. Conclusions: HLFs have a protective effect against DKD in rats. The underlying mechanism may involve the reduction of oxidative stress by inactivation of the p38MAPK signaling pathway in renal tissues.