20/03/2018
Perlindungan air Hidrogen Terhadap Penyakit Maag
Sakit maag disebabkan oleh beberapa hal, di antaranya akibat adanya lambung luka yang terbuka (tukak lambung). Selain itu bisa karena infeksi bakteri Helicobacter pylori, efek samping penggunaan obat anti inflamasi nonsteroid (OAINS), dan stres yang berkepanjangan.
Penyakit maagmerupakan keadaan rasa nyeri yang berasal dari lambung, usus halus, ataupun kerongkongan akibat beragam kondisi.
Umumnya sebagian besar penyakit lambung bisa disembuhkan tanpa konsultasi kepada dokter, akan tetapi proses pemeriksaan dokter medis diperlu apabila sakit maag disertai dengan sering muntah, sulit menelan, bahkan mengalami penurunan berat badan. Selain itu apabila Anda telah menginjak berusia 55 tahun ke atas.
Gejala Sakit Maag dan Cara Mengobati Asam Lambung
Berikut ini beberapa hal gejala asam lambung penyebab penyakit lambung :
Sakit Tukak lambung yaitu luka terbuka di lapisan dalam lambungEfek samping penggunaan obat anti-inflamasi nonsteroid (misalnya ibuprofen dan aspirin) dan obat golongan nitratInfeksi bakteri Helicobacter pyloriMasalah psikologi (misalnya cemas dan stres)Terlalu banyak makan dan makan terlalu cepatPenyakit pergerakan balik asam lambung menuju kerongkongan (refluks gastroesofagus)Mengonsumsi makanan berminyak, berlemak, dan pedasObesitas atau kegemukan MerokokTerlalu banyak mengonsumsi kafein, soda, atau minuman beralkoholTerlalu banyak mengonsumsi cokelatKonstipasi
Mengobati Sakit Maag
Sederhananya, cara mengobati sakit maag adalah menghidari penyebabnya, seperti menghentikan konsumsi zat kafein atau alkohol apabila sakit maag disebabkan oleh kedua zat tersebut. Segera hindari makanan-makanan yang bisa memicu sakit maag, ganti obat pereda nyeri sesuai saran dokter dan hindari stress.
Pengaruh Hidrogen Terhadap Sakit Maag
Ulserasi (luka terbuka yang sulit disembuhkan) sering terjadi sebagai akibat dari kejadian stres berat dan radikal hidroksil (⋅OH) yang merupakan salah satu faktor penyebab utamanya. Baru-baru ini, telah terbukti bahwa hidrogen, pengikat radikal hidroksi ⋅OH, secara efektif dapat melindungi hewan dari kerusakan jaringan akibat radikal bebas. Dengan cara yang sama, peneliti berhipotesis bahwa hidrogen mungkin memiliki efek perlindungan terhadap ulserasi karena stres. Ulserasi gaster atau tukak lambung adalah robeknya lapisan mukosa yang disebabkan oleh rusaknya ketahanan mukosa lambung.
Penelitian menggunakan tikus percobaan yang diinduksi dengan metode cold restraint stress. Penelitian menunjukkan bahwa perlakuan hidrogen mengurangi peroksidasi lipid akibat stres, karbonil protein dan oksidan DNA dan meningkatkan potensi jaringan antioksidan. Sebagai tambahan, hidrogen mengurangi respon inflamasi dan infiltrasi neutrofil dengan menekan aktivitas P-p38 MAPK, P-JNk dan NF-κB. Yang penting, hidrogen memperbaiki kerusakan mukosa lambung dengan mencegah apoptosis sel. Sebagai kesimpulan, pengobatan hidrogen secara efektif memperbaiki kerusakan mukosa lambung terkait stres melalui efek anti-oksidan, anti-inflamasi dan anti-apoptosisnya.
Informasi ini dikutip dari laporan resmi penelitian manfaat air hidrogen yang dikutip dari The protective of hydrogen on stress-induced gastric ulceration. Berikut laporan resminya :
Abstract :
Stress ulceration frequently occurs as a result of major stressful events and hydroxyl radical (⋅OH) is one of the major causative factors for it. Recently, it has been proved that hydrogen, a potent selectively ⋅OH scavenger, can effectively protect animals against ROS-induced tissue damage. In like manner, we hypothesize that hydrogen may have a protective effect against stress ulceration. Gastric ulceration was induced by the method of cold restraint stress. Rats in the hydrogen treatment group received hydrogen-rich saline (10 mL/kg body weight) 5 min before the stress. At 6h post-stress, gastric corpus mucosa was harvested for the measurement of malondialdehyde, protein carbonyl, 8-hydroxy-desoxyguanosine, glutathione, superoxide dismutase, myeloperoxidase, TNF-α, IL-1β and cytokine-induced neutrophils chemoattractant-1. In addition, western blotting was used to determine the expression of p38 MAPK, P-p38 MAPK, P-JNk, JNK, Bcl-xl, Bax and cleaved caspase-3. Nuclear translocation of NF-κB was assessed by electrophoretic mobility shift assay. Gastric mucosa structure and mucosal epithelial cells apoptosis were measured at 12h post-stress. Our present study showed that hydrogen treatment lessened the stress-induced lipid peroxidation, protein carbonyl and DNA oxidant and improved tissue antioxidant potential. In addition, hydrogen mitigated inflammatory response and neutrophils infiltration with suppressing the activity of P-p38 MAPK, P-JNk and NF-κB. Importantly, hydrogen ameliorated gastric mucosa damage with preventing cell apoptosis. Furthermore, the up-regulation of cleaved caspase-3, Bax and down-regulation of Bcl-xl expression were blocked by hydrogen treatment. In conclusion, hydrogen treatment effectively ameliorated stress-associated gastric mucosa damage via its anti-oxidant, anti-inflammatory and anti-apoptotic effects.
ABSTRACT Acute lung injury (ALI) is still a leading cause of morbidity and mortality in critically ill patients. Inhaled nitric oxide (NO) has been reported to ameliorate ALI. However, reactive nitrogen species produced by NO can cause lung injury. Because hydrogen gas (H2) is reported to eliminate peroxynitrite, it is expected to reduce the adverse effects of NO. Moreover, we have found that H2 inhalation can attenuate lung injury. Therefore, we hypothesized that combination therapy with NO and H2 might afford more potent therapeutic strategies for ALI. In the present study, a mouse model of ALI was induced by intratracheal administration of lipopolysaccharide (LPS). The animals were treated with inhaled NO (20 ppm), H2 (2%), or NO + H2, starting 5 min after LPS administration for 3 h. We found that LPS-challenged mice exhibited significant lung injury characterized by the deterioration of histopathology and histologic scores, wet-to-dry weight ratio, and oxygenation index (ratio of oxygen tension to inspired oxygen fraction [Pao2/Fio2]), as well as total protein in the bronchoalveolar lavage fluid (BALF), which was attenuated by NO or H2 treatment alone.
RESULT Combination therapy with NO and H2 had a more beneficial effect with significant interaction between the two. While the nitrotyrosine level in lung tissue was prominent after NO inhalation alone, it was significantly eliminated after breathing a mixture of NO with H2. Furthermore, NO or H2 treatment alone markedly attenuated LPS-induced lung neutrophil recruitment and inflammation, as evidenced by downregulation of lung myeloperoxidase activity, total cells, and polymorphonuclear neutrophils in BALF, as well as proinflammatory cytokines (tumor necrosis factor α, interleukins 1β and 6, and high-mobility group box 1) and chemokines (keratinocyte-derived chemokine, macrophage inflammatory proteins 1α and 2, and monocyte chemoattractant protein 1) in BALF. Combination therapy with NO and H2 had a more beneficial effect against lung inflammatory response. Moreover, combination therapy with NO and H2 could more effectively inhibit LPS-induced pulmonary early and late nuclear factor κB activation as well as pulmonary cell apoptosis. In addition, combination treatment with inhaled NO and H2 could also significantly attenuate lung injury in polymicrobial sepsis.
CONCLUSION Combination therapy with subthreshold concentrations of NO and H2 still had a significantly beneficial effect against lung injury induced by LPS and polymicrobial sepsis. Collectively, these results demonstrate that combination therapy with NO and H2 provides enhanced therapeutic efficacy for ALI.
