The neuroprotective effect of transforming growth factor-beta1 via anti-apoptosis on hypoxic-ischemic brain injury in neonatal rats / 대한주산의학회잡지

OBJECTIVE: TGF-beta1 is an important neuronal survival factor to neurons from damage induced by cerebral ischemia. We examined whether treatment with the TGF-beta1 has neuroprotective effects on HI brain injury in neonatal rats using Rice-Vannucci model (in vivo) and in rat brain cortical cell culture induced by hypoxia (in vitro). METHODS: Seven-day-old Sprague-Dawley (SD) rat pups were subjected to left carotid occlusion followed by 2 hour of hypoxic exposure. At the before and after 30 minutes of HI, the animals were injected intracerebrally with TGF-beta1 0.5 ng/kg. In addition, brain cortical cell culture model using pregnant SD rats for 19 days were experimented and induced for hypoxia cell injury. The cell were treated with TGF-beta1 1 ng/mL, 5 ng/mL and 10 ng/mL separately. and incubated in 1% O2 incubator. Apoptosis was measured in the injured hemispheres 7 days after the HI insults using western blot for pro-apoptotic marker-bax, caspase-3 and anti-apoptotic marker-Bcl-2. RESULTS: In western blot and real-time PCR showed Caspase-3, Bax and Bax/Bcl-2 levels was reduced and Bcl-2 level was increased in vivo. In brain cortical cell culture, Bcl-2 expression was greater in the group with low dose of TGF-beta1 (1 ng/mL) in western blot. CONCLUSION: This study thus suggests that the neuroprotective role of TGF-beta1 against HI brain injury is mediated through an anti-apoptotic effect, which offers the possibility of TGF-beta1 application for the treatment of neonatal HI encephalopathy.

A Case of Esophageal Achalasia in a 10-Year-Old Girl with Persistent Asthma / 소아알레르기및호흡기학회지

Achalasia is a primary esophageal motor disorder, which is a rare disease with an estimated prevalence of 0.5-1 per 100,000 general population. The typical symptoms are vomiting, dysphagia and weight loss, but the respiratory symptoms are often presented in the 20-30% of the patients. The respiratory symptoms are known to be caused by the regurgitation or aspiration of the undigested food. Choking, recurrent pneumonia nocturnal cough are common and bronchiectasis, lung abscess and atelectasis also have been reported. The treatment of achalasia aimed at improving esophageal peristalsis by reducing pressure at the lower esophageal sphincter. We experienced a case of esophageal achalasia coincidentally found in a 10-year-old girl who was admitted with the exacerbation of asthma. She had pneumatic dilatation and her asthma symptoms including nocturnal cough much improved.

The Cardioprotective Effects of Resveratrol via Anti-Apoptosis in Hypoxic Injury of Myocardial Cells

BACKGROUND AND OBJECTIVES: Resveratrol (trans-3, 4', 5-trihydroxy-stilbene), a naturally occurring polyphenolic phytoalexin found abundantly in grape skins and red wines, has been reported to protect heart cells from ischemia/reperfusion (I/R) injury through its significant antioxidant properties. Apoptosis of cardiac myocytes is also involved in several cardiovascular diseases, but it remains unknown whether the protective effects of resveratrol in hypoxic myocardial cell injury are mediated via suppression of apoptosis. In this study, we investigated whether resveratrol confers cardioprotection against hypoxia via anti-apoptosis in a hypoxic model of cultured H9c2 cardiomyoblasts. MATERIALS AND METHODS: H9c2 cardiomyoblasts were obtained from the Korean Cell Line Bank. The cultured cells were divided into four groups: a normal control group, a hypoxia group, a group treated with resveratrol (10 microgram/mL) before hypoxic insult, and a group treated with resveratrol (10 microgram/mL) after hypoxic insult. The control group was placed in 5% CO2 incubators, and the hypoxia and resveratrol-treated groups were placed in 1% O2 incubators. Apoptosis was assayed by cytological analysis with Western blotting and real-time PCR for Bcl-2, Bax, and caspase-3. RESULTS: The expression of Bcl-2 was significantly decreased in the hypoxia group compared with the control group, and resveratrol treatment inhibited the hypoxia-induced decline of Bcl-2 in hypoxic myocardial cells. Conversely, the expressions of Bax and caspase-3 were significantly increased in the hypoxia group, while resveratrol inhibited the hypoxia-induced increase of Bax and caspase. In addition, hypoxia significantly increased the ratio of Bax/Bcl-2 expression, but it was significantly decreased in the resveratrol-treated group. CONCLUSION: The present study demonstrates that the cardioprotective effects of resveratrol in hypoxic injury are mediated via the mechanisms of anti-apoptosis.