Effects of newborn intraoral pressure on colostrum intake / Efeito da pressão intraoral de recém-nascidos na ingestão de colostro

ABSTRACT Objective To explore the effects of intraoral pressure on colostrum intake. Methods Healthy women with full-term infants were admitted in the study after birth. Intraoral pressure was detected before and after the mothers' onset of lactation by a pressure sensor during a breastfeeding session. Colostrum intake was measured by weighting the infant before and after breastfeeding. The onset of lactation was confirmed by the mothers' perceptions of sudden breast fullness. Results The newborns' peak sucking pressure was 19.89±7.67kPa before the onset of lactation, dropping to 11.54±4.49kPa after mothers' onset of lactation (p<0.01). The colostrum intake was 4.02±4.26g before the onset of lactation, and 11.09±9.43g after the onset of lactation. Sucking pressure was correlated with the amount of colostrum intake before and after the onset of lactation after adjusting the confounding factors. Conclusions The newborns' intraoral pressure at early stage played a predominant role in colostrum intake. It is recommended to initiate breastfeeding immediately after the birth to take advantages of the active and robust sucking response. It is valuable to understand the importance that the sucking pressure plays in the colostrum intake and active immunity achievement during the first several days after birth.

RESUMO Objetivo Explorar o efeito das pressões intraorais na ingestão de colostro. Métodos Mulheres saudáveis com bebês a termo foram matriculadas após o nascimento. As pressões intraorais foram detectadas antes e após o início da lactação pelas mães através de um sensor de pressão durante uma sessão de amamentação. A ingestão de colostro foi mensurada pelo peso da criança antes e após a amamentação. O início da lactação foi confirmado pela percepção das mães de plenitude súbita da mama. Resultados O pico de pressão de sucção dos recém-nascidos foi de 19,89±7,67kPa antes do início da lactação e caiu para 11,54±4,49kPa após o início da lactação (p<0,01). A ingestão de colostro foi de 4,02±4,26g antes do início da lactação e 11,09±9,43g após o início da lactação. A pressão de sucção foi correlacionada com a quantidade de ingestão de colostro antes e após o início da lactação depois de terem sido feitos ajustes dos fatores de confusão. Conclusão A pressão intraoral dos recém-nascidos no estágio inicial teve um papel predominante na ingestão de colostro. Recomenda-se iniciar a amamentação imediatamente após o nascimento para aproveitar as vantagens da resposta ativa e robusta à sucção. É importante entender a importância que a pressão de sucção desempenha na ingestão de colostro e na conquista da imunidade ativa durante os primeiros dias após o nascimento.

Studies on the mechanism of SIRT1/AMPK signaling pathway between hepatocytes and hepatic stellate cells / 中国药理学与毒理学杂志

OBJECTIVE To investigate the mechanism of SIRT1/AMPK signaling pathway between hepatocytes and hepatic stellate cells (HSCs). METHODS Normal human Chang liver cells and human hepatic stellate cell line, LX-2 cells were treated with SRT1720 (10 μmol·L-1) and AICAR (500 μmol·L-1) prior to ethanol (50 mmol·L-1) for 24 and 48 h. Cell viability was analyzed by methyl thiazolyl tetrazolium assay. SIRT1, AMPK and p-AMPK mRNA levels for 24 h and 48 h were analyzed by RT-PCR, SIRT1, AMPK and p-AMPK protein expressions in the supernatant at 24 and 48 h was detected by Western blot. RESULTS SRT1720 and AICAR effectively decreased LX-2 cell viabilities and exhibited scarcely little toxicity in human Chang liver cells. SRT1720 and AICAR attenuated collagen-I, α-smooth muscle actin (α-SMA) levels, activated liver kinase B-1 (LKB1) and AMPK phosphorylation in ethanol treated LX-2 cells. Meanwhile, SRT1720 and AICAR enhanced SIRT1 expression mediated by ethanol both in Chang liver cells and LX-2 cells. Furthermore, SRT1720 and AICAR suppressed the expression of sterol regulatory element-binding protein-1 (SREBP-1) to regulate fatty acid synthesis. CONCLUSION SIRT1 agonist and AMPK agonist blocked the crosstalk between hepatocytes and HSCs via SIRT1/AMPK signaling pathway to modulate hepatocytes accumulation of lipid and HSCs activation.

Hepato-protective effect of thymoquinone against acetaminophen induced liver injury is associated with regulation of JNK and AMPK signaling pathway / 中国药理学与毒理学杂志

OBJECTIVE To investigate the hepato-protective mechanism of thymoquinone (TQ) onthe development of acetaminophen (APAP)- induced liver injury. METHODS In vivo, male kunming mice were injected with a single dose of 300 mg·kg-1 APAP. Some mice were pretreated with TQ (5 or 20 mg·kg-1) and N-acetylcysteine (NAC, 300 mg·kg-1) 2 h before APAP injection. Mice were euthanized at 2 h, 6 h, 12 h after APAP treatment. In vitro, human Chang liver cells were incubated with 3.125, 6.25 or 12.5 μmol·L-1 TQ, 10 μmol·L-1 SP600125 and 500 μmol·L-1 AICAR in the presence of APAP for 24 h. Cell viability were analyzed by MTT assay, protein expressions were assessed by Western blot. RESULTS TQ pretreatment significantly reduced serum aminotransferase and increased hepatic gluta?thione (GSH) and glutathione peroxidase (GSH-PX) activities, while significantly inhibited interleukin-1β(IL-1β) levels. TQ significantly inhibited c-Jun N-terminal kinase (JNK), extracellular signal regulated kinase (ERK) and P38 phosphorylation induced by APAP. Moreover, TQ inhibited phosphatidylinositol 3- kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling activation and activated AMPK phosphorylation induced by APAP. In addition, TQ inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation on APAP-induced liver injury. In vitro, APAP enhanced JNK phosphorylation and attenuated AMPK phosphorylation in Chang liver cells, and these effects were blocked by pretreatment with TQ, SP600125 (JNK inhibitor) and AICAR (AMPK activator). CONCLUSION Our findings suggest that TQ may actively prevent APAP-induced liver injury, and this effect may be mediated by JNK and AMPK signaling pathways.