scholarly journals Pengaruh Pemberian Minuman Beralkohol (Ciu) Terhadap Histomorfometri Ren Mencit (Mus musculus L.)

2021 ◽  
Vol 6 (2) ◽  
pp. 146-153
Author(s):  
Aida Ridwanah Yusuf ◽  
Silvana Tana ◽  
Tyas Rini Saraswati

Ciu merupakan salah satu minuman beralkohol yang banyak dikonsumsi oleh masyarakat Indonesia. Konsumsi Ciu dapat merusak jaringan dan organ tubuh, karena hasil metabolisme alkohol merupakan molekul reaktif yang berupa Reactive Oxygen Species (ROS). Penelitian bertujuan untuk menganalisis pengaruh konsumsi Ciu terhadap perubahan histomorfologi ren. Penelitian menggunakan 15 ekor mencit jantan dengan Desain Rancangan Acak Lengkap dengan 3 kelompok perlakuan dan 5 ulangan, yaitu T0: mencit tidak diberikan perlakuan Ciu, T1: mencit diberi perlakuan Ciu 1 x 0,2ml/hari, dan T2: mencit diberi perlakuan Ciu 2 x 0,2ml/hari. Parameter pengukuran antara lain bobot ren, diameter glomerulus, lebar ruang Bowman, ukuran sel epitel dan diameter lumen tubulus kontortus proksimal, dan ukuran sel epitel dan diameter lumen tubulus kontortus distal. Data yang diperoleh dianalisis menggunakan uji Analysis of Variance (ANOVA), dilanjutkan dengan uji Duncanpada taraf kepercayaan 95%. Hasil penelitian menunjukkan bahwa pemberian Ciu memberikan pengaruh nyata (P<0,05) terhadap bobot ren, ukuran sel epitel tubulus kontortus proksimal, dan diameter lumen tubulus kontortus distal. Kesimpulan, pemberian Ciu pada mencit dapat merubah histomorfometri dan menurunkan bobot ren. Ciu is one of an alcoholic beverages that widely consumed by Indonesian people. Ciu consumption could damage body tissues and organs, because the result of alcohol metabolism is a reactive molecule that forms Reactive Oxygen Species (ROS). The study aims to analyze the effect of Ciu consumption on ren histomorphometry changes. The study used 15 male mice with Completed Random Design with 3 treatment groups and 5 repetitions, i.e. T0: mice were not given Ciu treatment, T1: mice were treated with Ciu 1 x 0,2ml/day, T2: mice were treated with Ciu 2 x 0,2ml/day. The measurement parameters are ren weight, glomerular diameter, Bowman space width, epithelial cell size and lumen diameter of proximal tubules, and epithelial cell size and lumen diameter of distal tubules. Data obtained were analyzed using the Analysis of Variance (ANOVA) test, followed by Duncan’s test at 95% confidence level. The result of the study showed that giving Ciu had a significant effect on ren weight (P<0,05), epithelial cell size of proximal tubule, and lumen diameter of distal tubule. In conclusion, Ciu given to mice could change the histomorphometry and decrease weight of its ren.

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 1257-1268 ◽  
Author(s):  
C. Schell ◽  
M. Albrecht ◽  
S. Spillner ◽  
C. Mayer ◽  
L. Kunz ◽  
...  

The wall of the seminiferous tubules contains contractile smooth-muscle-like peritubular cells, thought to be important for sperm transport. Impaired spermatogenesis in men typically involves remodeling of this wall, and we now found that smooth muscle cell (SMC) markers, namely myosin heavy chain (MYH11) and smooth muscle actin (SMA) are often lost or diminished in peritubular cells of testes of men with impaired spermatogenesis. This suggests reduced contractility of the peritubular wall, which may contribute to sub- or infertility. In these cases, testicular expression of cyclooxygenase-2 (COX-2) implies formation of prostaglandins (PGs). When screening different PGs for their ability to target human testicular peritubular cells (HTPCs), only a PG metabolite, 15-deoxy-Δ12-14-prostaglandin-J2 (15dPGJ2), was effective. In primary cultures of HTPCs, 15dPGJ2 increased cell size in a reversible manner. Importantly, 15dPGJ2 treatment resulted in a loss of typical differentiation markers for SMCs, namely MYH11, calponin, and SMA, whereas fibroblast markers were unchanged. Collagen gel contraction assays revealed that this loss correlates with a reduced ability to contract. Experiments with an antagonist (bisphenol A diglycidyl ether) and agonist (troglitazone) for a cognate 15dPGJ2 receptor (i.e. peroxisome proliferator-activated receptor-γ) indicated that peroxisome proliferator-activated receptor-γ is not directly involved. Rather, the mode of action of 15dPGJ2 involves reactive oxygen species. The antioxidant N-acetylcysteine not only blocked ROS formation but also prevented the increase in cell size and the loss of contractility in HTPCs challenged with 15dPGJ2. We conclude that 15dPGJ2, via reactive oxygen species, influences SMC phenotype and contractility of human peritubular cells and possibly is involved in the development of human male sub-/infertility.


2006 ◽  
Vol 26 (12) ◽  
pp. 4701-4711 ◽  
Author(s):  
Courtney G. Havens ◽  
Alan Ho ◽  
Naohisa Yoshioka ◽  
Steven F. Dowdy

ABSTRACT Proliferating cells have a higher metabolic rate than quiescent cells. To investigate the role of metabolism in cell cycle progression, we examined cell size, mitochondrial mass, and reactive oxygen species (ROS) levels in highly synchronized cell populations progressing from early G1 to S phase. We found that ROS steadily increased, compared to cell size and mitochondrial mass, through the cell cycle. Since ROS has been shown to influence cell proliferation and transformation, we hypothesized that ROS could contribute to cell cycle progression. Antioxidant treatment of cells induced a late-G1-phase cell cycle arrest characterized by continued cellular growth, active cyclin D-Cdk4/6 and active cyclin E-Cdk2 kinases, and inactive hyperphosphorylated pRb. However, antioxidant-treated cells failed to accumulate cyclin A protein, a requisite step for initiation of DNA synthesis. Further examination revealed that cyclin A continued to be ubiquitinated by the anaphase promoting complex (APC) and to be degraded by the proteasome. This antioxidant arrest could be rescued by overexpression of Emi1, an APC inhibitor. These observations reveal an intrinsic late-G1-phase checkpoint, after transition across the growth factor-dependent G1 restriction point, that links increased steady-state levels of endogenous ROS and cell cycle progression through continued activity of APC in association with Cdh1.


2005 ◽  
Vol 289 (2) ◽  
pp. H947-H959 ◽  
Author(s):  
Dan Chalothorn ◽  
Hua Zhang ◽  
Jason A. Clayton ◽  
Steven A. Thomas ◽  
James E. Faber

Catecholamine stimulation of α1-adrenoceptors exerts growth factor-like activity, mediated by generation of reactive oxygen species, on arterial smooth muscle cells and adventitial fibroblasts and contributes to hypertrophy and hyperplasia in models of vascular injury and disease. Adrenergic trophic activity also contributes to flow-mediated positive arterial remodeling by augmenting proliferation and leukocyte accumulation. To further examine this concept, we studied whether catecholamines contribute to collateral growth and angiogenesis in hindlimb insufficiency. Support for this hypothesis includes the above-mentioned studies, evidence that ischemia augments norepinephrine release from sympathetic nerves, and proposed involvement of reactive oxygen species in angiogenesis and collateral growth. Mice deficient in catecholamine synthesis [by gene deletion of dopamine β-hydroxylase (DBH−/−)] were studied. At 3 wk after femoral artery ligation, increases in adductor muscle perfusion were similar in DBH−/− and wild-type mice, whereas recovery of plantar perfusion and calf microsphere flow were attenuated, although not significantly. Preexisting collaterals in adductor of wild-type mice showed increases in lumen diameter (60%) and medial and adventitial thickness (57 and 119%, P < 0.05 here and below). Lumen diameter increased similarly in DBH−/− mice (52%); however, increases in medial and adventitial thicknesses were reduced (30 and 65%). Leukocyte accumulation in the adventitia/periadventitia of collaterals was 39% less in DBH−/− mice. Increased density of α-smooth muscle actin-positive vessels in wild-type adductor (45%) was inhibited in DBH−/− mice (2%). Although both groups experienced similar atrophy in the gastrocnemius (∼22%), the increase in capillary-to-muscle fiber ratio in wild-type mice (21%) was inhibited in DBH−/− mice (7%). These data suggest that catecholamines may contribute to collateral growth and angiogenesis in tissue ischemia.


Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 477
Author(s):  
Panfeng Fu ◽  
Ramaswamy Ramchandran ◽  
Tara Sudhadevi ◽  
Prasanth P.K. Kumar ◽  
Yashaswin Krishnan ◽  
...  

Pseudomonas aeruginosa (PA) infection increases reactive oxygen species (ROS), and earlier, we have shown a role for NADPH oxidase-derived ROS in PA-mediated lung inflammation and injury. Here, we show a role for the lung epithelial cell (LEpC) NOX4 in PA-mediated chromatin remodeling and lung inflammation. Intratracheal administration of PA to Nox4flox/flox mice for 24 h caused lung inflammatory injury; however, epithelial cell-deleted Nox4 mice exhibited reduced lung inflammatory injury, oxidative stress, secretion of pro-inflammatory cytokines, and decreased histone acetylation. In LEpCs, NOX4 was localized both in the cytoplasmic and nuclear fractions, and PA stimulation increased the nuclear NOX4 expression and ROS production. Downregulation or inhibition of NOX4 and PKC δ attenuated the PA-induced nuclear ROS. PA-induced histone acetylation was attenuated by Nox4-specific siRNA, unlike Nox2. PA stimulation increased HDAC1/2 oxidation and reduced HDAC1/2 activity. The PA-induced oxidation of HDAC2 was attenuated by N-acetyl-L-cysteine and siRNA specific for Pkc δ, Sphk2, and Nox4. PA stimulated RAC1 activation in the nucleus and enhanced the association between HDAC2 and RAC1, p-PKC δ, and NOX4 in LEpCs. Our results revealed a critical role for the alveolar epithelial NOX4 in mediating PA-induced lung inflammatory injury via nuclear ROS generation, HDAC1/2 oxidation, and chromatin remodeling.


Biomedika ◽  
2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Warigit Dri Atmoko ◽  
Bambang Purwanto ◽  
Sugiarto Sugiarto

Lupus nefritis (LN) terkait dengan penebalan membran basal glomerulus. Pengendapan kompleks imun  memicu kaskade respon inflamasi disertai aktivasi reactive oxygen species (ROS), kemudian menyebabkan fibrosis yang mendorong terjadinya kerusakan ginjal. Interleukin 17 merupakan sitokin yang sangat berperan pada reaksi inflamasi tipe-lambat. Produksinya dipicu oleh peningkatan produksi kemokin oleh sejumlah jaringan untuk merekrut monosit dan netrofil ke sisi inflamasi. IL-17 diproduksi sel Th17 dan diinduksi oleh IL-23. IL-17 berespon terhadap invasi patogen ekstraseluler dan menginduksi perusakan matriks seluler patogen. IL-17 akan merangsang sel B untuk memproduksi dan mensekresikan autoantibodi, selanjutnya akan terbentuk kompleks atigen-autoantibodi. Kompleks antigen-autoantibodi yang berada di sirkulasi akhirnya akan terdisposisi pada sel target, termasuk sel fibroblas, sel mesangial, podosit, sel tubulus dan sel endotel di glomerulus. Kompleks ini akan menyebabkan terjadinya glomerulosklerosis dan fibrosis interstisial pada ginjal, kemudian selanjutnya menyebabkan kerusakan pada ginjal dan terjadilah mikroalbuminuria. Disamping itu, akan terjadi disfungsi endotel kapiler glomerulus yang akan menyebabkan albuminuria. Suplemen N-asetil sistein (NAS) pada lupus nefritis dapat mengurangi efek nefrotoksik pada ginjal, melalui penurunan ekspresi IL-17 dan derajat fibrosis interstisial. Penelitian ini merupakan penelitian eksperimental laboratoris, dengan sampel 24 ekor mencit Balb/C betina yang dibagi menjadi kelompok kontrol, LN, dan LN+NAS. Untuk membuat model LN, hewan coba diberikan injeksi 0,5 ml pristan intraperitoneal dosis tunggal. NAS diberikan secara peroral dengan dosis 4,7 mg/hari (setara dengan dosis manusia 1.800 mg) selama delapan minggu. Ekspresi IL-17 diperiksa secara imunohistokimia dengan antibodi monoklonal terhadap IL-17. Cara ukur dinilai secara kuantitatif, dihitung jumlah sel positif IL17 terhadap 100 sel, secara visual dengan mikroskop cahaya pembesaran 400 x. Penilaian fibrosis interstisial ditentukan secara kuantitatif dengan cara mengukur tebal jaringan interstisial dengan menggunakan micrometer yang telah dikalibrasi pada pembesaran 400 x. Analisis data menggunakan analysis of variance (Anova) dan untuk menentukan perbedaan kemaknaan digunakan p<0,05. Hasil Penelitian menunjukkan bahwa pemberian NAS menurunkan ekspresi IL-17 (23,8±14,1 vs 10,6±6,8 per 100 sel netrofil imunoreaktif; p =0,042)  dan menurunkan fibrosis interstisial (22,3±5,7 vs 15,5±5,4; p =0,030) dibandingkan kelompok LN. Berdasarkan penelitian ini dapat disimpilkan bahwa NAS secara bermakna menurunkan ekspresi IL-17 dan fibrosis interstisial ginjal pada mencit model LN.Kata Kunci: fibrosis interstisial, lupus nefritis, interleukin 17, pristan


2013 ◽  
Vol 32 (2) ◽  
pp. 417-430 ◽  
Author(s):  
Joshua Y. Lee ◽  
Simon A. Hirota ◽  
Louise E. Glover ◽  
Glen D. Armstrong ◽  
Paul L. Beck ◽  
...  

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