Rat Muscle Research Articles

Muscle Tissue Response to Vipera berus berus and Vipera berus nikolskii Venoms: A Study on Matrix Metalloproteinases and Cytokine Modulation

Vipera berus, also known as the common adder, is a snake species widely distributed in Europe and parts of Asia. Its venom is a mix of enzymatic and non-enzymatic components causing both local and systemic effects including edema, hemorrhage, myonecrosis, gastrointestinal disorders, and rarely – rhabdomyolysis, coagulopathy and hypovolemic shock. Matrix metalloproteinases (MMPs) and cytokines, being inflammatory mediators, participate both in the development of these reactions and in tissue regeneration after acute damage. The current study was aimed at analyzing the concentrations of important mediators of tissue damage, inflammation and regeneration, namely, MMP-1, -2, -3, -8, -10, TIMP-1 (a tissue inhibitor of MMPs), and pro- and anti-inflammatory cytokines, in rat muscle after intraperitoneal injection of venoms from two subspecies of adders – V. berus berus and V. berus nikolskii — to clarify their role in the local response of skeletal muscle to the studied venoms. Changes in muscle tissue were revealed, namely, significant increase in almost all MMPs including MMP-2, as well as TIMP-1, IFN-γ and anti-inflammatory IL-4 and IL-10 content. Moreover, a tendency for some pro-inflammatory cytokines levels to decline 24 h after venom administration was observed, which may be a sign of inflammation suppression and the beginning of reparative processes associated with extracellular matrix remodeling and formation of an optimal environment for muscle regeneration. However, to establish the exact mechanisms of the changes we found, further studies are needed. The ability of V. berus nikolskii venom to induce more pronounced changes was also shown. Our results may be useful for the development of differentiated and more effective treatment strategies for the consequences of bites by these snakes, which include myonecrosis

Acute high-intensity muscle contraction moderates AChR gene expression independent of rapamycin-sensitive mTORC1 pathway in rat skeletal muscle.

The relationship between mechanistic target of rapamycin complex 1 (mTORC1) activation after resistance exercise and acetylcholine receptor (AChR) subunit gene expression remains largely unknown. Therefore, we aimed to investigate the effect of electrical stimulation-induced intense muscle contraction, which mimics acute resistance exercise, on the mRNA expression of AChR genes and the signalling pathways involved in neuromuscular junction (NMJ) maintenance, such as mTORC1 and muscle-specific kinase (MuSK). The gastrocnemius muscle of male adult Sprague-Dawley rats was isometrically exercised. Upon completion of muscle contraction, the rats were euthanized in the early (after 0, 1, 3, 6 or 24h) and late (after 48 or 72h) recovery phases and the gastrocnemius muscles were removed. Non-exercised control animals were euthanized in the basal state (control group). In the early recovery phase, Agrn gene expression increased whereas LRP4 decreased without any change in the protein and gene expression of AChR gene subunits. In the late recovery phase, Agrn, Musk, Chrnb1, Chrnd and Chrne gene expression were altered and agrin and MuSK protein expression increased. Moreover, mTORC1 and protein kinase B/Akt-histone deacetylase 4 (HDAC) were activated in the early phase but not in the late recovery phase. Furthermore, rapamycin, an inhibitor of mTORC1, did not disturb changes in AChR subunit gene expression after muscle contraction. However, rapamycin addition slightly increased AChR gene expression, while insulin did not impact it in rat L6 myotube. These results suggest that changes in the AChR subunits after muscle contraction are independent of the rapamycin-sensitive mTORC1 pathway.

Effect of skeletal muscle immobilization on regional anisotropic viscohyperelastic properties change in a rat model

Passive mechanical properties in three different zones (distal, proximal, and medial) of biceps brachii immobilized in short position and its free contralateral were investigated. For that, in vitro equibiaxial relaxation tests were performed with samples harvested from skeletal muscles of immobilized rats during one or two weeks. From data obtained in two plane axes of loading, a viscohyperelastic anisotropic model described by a strain energy function coupled with second order Maxwell's model, was used to identify the material parameters. It has been shown that the zone influences the material parameters of the hyperelasticity behavior while the immobilization acts rather on the viscoelasticity response. Based on measurements of histological parameters from flexor carpi ulnaris muscles, we observed that immobilization produced contractile tissue atrophy and connective tissue thickening. The muscle atrophy caused by immobilization could lead to a more linear mechanical behavior along the axis of the muscle fibers. Furthermore, fibrosis, quantified by histological analysis on flexor carpi ulnaris muscles, could result in highly non-linear behavior along the other axis. These structural changes also contribute to an increase in relaxation following immobilization along both axes (+11.7% and +15.5% on average with p < 0.001 and p < 0.01 respectively for each axis). Statement of significanceTo our best knowledge, this work is the first to investigate the anisotropic, viscohyperelastic and heterogeneous properties within a passive skeletal muscle immobilized in a short position. For that, from a rat model, equibiaxial relaxation tests were performed and material parameters were found from a strain energy function coupled with a Maxwell's model. We showed that excising zone of samples greatly influences the parameters of the hyperelastic behavior while the immobilization influences the viscoelasticity response instead. Furthermore, histological analysis permitted to quantify fibrosis in the skeletal muscle and bear out, at least in part, changes in relaxation behavior following immobilization.

Beneficial effects of the SGLT2 inhibition on oxidative skeletal muscle in infarcted rats

Abstract Introduction Metabolic, morphological, and biochemical changes in skeletal muscle are common in chronic heart failure patients. Despite the cardioprotective effects of sodium-glucose co-transporter 2 (SGLT2) inhibition in heart failure, the impact of this drug on skeletal muscle remains poorly understood. This study investigated the effects of SGLT2 inhibitor empagliflozin (EMPA) on the soleus muscle of rats with myocardial infarction (MI)-induced heart failure. Methods One week after MI induction, male Wistar rats were divided into Sham (n=10), Sham+EMPA (n=12), MI (n=10) and MI+EMPA (n=09) groups. EMPA was added to rat chow (5 mg/kg/day) for 12 weeks. Cardiac remodeling was evaluated by echocardiogram. Enzymatic activity and oxidative stress marker concentrations were assessed by spectrophotometry; protein expression was evaluated by Western blotting. After histological analysis of the left ventricle (LV), only rats with MI greater than 35% of total LV area were included in the study. Statistical analysis: ANOVA and Tukey or Kruskal–Wallis and Dunn and t test; p&amp;lt;0.05. Results Infarction size did not differ between groups. Infarcted groups had larger LV systolic and diastolic diameters, LV diastolic area (Sham 47±7.1; Sham+EMPA 48±4.5; MI 100±16.1*; MI+EMPA 85±10.1#† mm2; p&amp;lt;0.05: * vs Sham; # vs Sham+EMPA; † vs MI), and left atrial diameter (Sham 5.62±0.2; Sham+EMPA 5.65±0.3; MI 7.69±1.3*; MI+EMPA 6.85±0.9#† mm; p&amp;lt;0.05: * vs Sham; # vs Sham+EMPA; † vs MI); and lower LV posterior wall shortening velocity and ejection fraction than control groups. Echocardiographic changes were attenuated in MI+EMPA compared to MI. Other results are shown in Picture 1. Conclusion SGLT2 inhibitor empagliflozin attenuates infarction-induced cardiac remodeling in rats. Empagliflozin prevents increase in oxidative stress, modulates protein turnover by IGF-1 pathway, and attenuates morphological and biochemical changes in the soleus muscle of infarcted rats.

Photobiomodulation and Physical Exercise Modulate of Cell Survival Proteins in the Skeletal Muscle of Rats with Heart Failure and Diabetes Mellitus.

Introduction: Heart failure (HF) and type 2 diabetes mellitus (DM2) are global health problems that often lead to muscle atrophy. These conditions are associated with increased autophagy and apoptosis in the muscle cells, resulting in decreased muscle mass. Physical exercise associated with photobiomodulation (PBM) seems promising to attenuate the skeletal muscle changes caused by HF and DM2, due to its direct effects on mitochondria, which may result in an increase in antioxidant capacity. Objective: To verify the influence of physical exercise and the association with PBM on autophagy, apoptosis, and cell survival signaling pathways in myocytes from rats with HF and DM2. Materials and Methods: Male rats were assigned to one of four groups: control (CT), HF+DM (disease model), exercise+HF+DM (EX+HF+DM), and EX+HF+DM+PBM (EX+HF+DM+PBM). To induce DM2, we administered streptozotocin (STZ) (0.25 mL/kg, intraperitoneally). HF was induced by coronary ligation. One week post-induction, an 8-week aerobic exercise and PBM protocol was initiated. Western blot analysis was used to measure the expression of apoptosis-related proteins and autophagy. Results: The EX+HF+DM+PBM group showed a substantial increase in Nrf2, p-AKT, and LC3-I levels compared to the HF+DM group. Conclusions: These findings suggest that physical exercise combined with PBM can upregulate proteins that promote myocyte survival in rats with HF and DM2.

The Effect of “Carvacrol” on Ischemia-Reperfusion Injury in the Skeletal Muscles of Rats

The Effect of “Carvacrol” on Ischemia-Reperfusion Injury in the Skeletal Muscles of Rats

Rotigaptide inhibits spontaneous contractions of gastric smooth muscle in diabetic rats via the PKCα-Cx43 pathway.

The study aimed to investigate the effect of rotigaptide (ZP123) on spontaneous contractions of gastric smooth muscle in diabetic rats and explore the underlying mechanisms. Twelve rats were randomly divided into model and normal control groups. Changes in gastric smooth muscle spontaneous contractions in each group were observed. Western blot analysis was performed to detect Cx43 and PKCα expression. Rat gastric smooth muscle cells were cultured in vitro and divided into normal glucose, high glucose and high glucose+rotigaptide group. The intracellular Ca2+ content was observed by immunofluorescence. The amplitude and frequency of gastric smooth muscle spontaneous contractions were reduced in the model group than the normal control group (all p < .01), which were reduced after rotigatide treatment than before treatment in the model group (all p < .01). The model+rotigaptide group showed decreased membrane expression of Cx43, increased cytoplasmic expression of Cx43, increased membrane expression of p-PKCα Thr497 and lower membrane/cytoplasm ratio of Cx43 expression compared with the model group (all p < .01). The intracellular Ca2+ content was increased in the high glucose group than the normal glucose group (p < .01), while no significant difference was observed between the high glucose+rotigaptide and high glucose groups. Our findings suggest that rotigatide can stabilize the intracellular Ca2+ concentration in gastric smooth muscle cells under high glucose condition by upregulating PKCα activity and downregulating the number of GJs and the opening rate of GJ hemichannels through the PKCα-Cx43 pathway, thus inhibiting spontaneous contractions of gastric smooth muscle in diabetic rats.

Alterations in FoxO3a, NF-κB, and MuRF1 Expression in the Soleus Muscle of Male Rats Following High-Intensity Interval Training and Detraining.

Activation of the transcription factors FoxO3a and NF-κB is necessary for muscle atrophy, which occurs during cancer cachexia and detraining. It is not known how high-intensity interval training (HIIT) and detraining affect activation of these pathways. Two-month-old male Sprague-Dawley rats were assigned to sedentary control (SC) (n = 6) and HIIT (HIIT) (n = 18) groups. The HIIT group was divided into three subgroups: HIIT (n = 6), HIIT + 7-day detraining (n = 6), and HIIT + 14-day detraining (n = 6). The expression of FoxO3a, NF-κB, MuRF1, and PGC-1α in the soleus muscle was examined by RT-PCR using CYBR Green. The 2-Ct, Livak method was used to calculate the changes in data expression. The soleus muscle mass increased after HIIT (35.10%) and decreased after 7- and 14-day of detraining (15 and 21%, respectively). The mRNA expression levels of NF-κB, MuRF1, and PGC1α in the soleus muscle were upregulated, and FoxO3a levels were significantly lower in the HIIT group compare to the SC group (p = 0.001). Taken together, the activity of the FoxO3a/MuRF1 pathway, but not NF-κB /MuRF1, can promote atrophy due to detraining, and MuRF1 is not always a good marker of atrophy.

Mechanical Stress-Oxidative Stress Axis: Biological Basis in the Vaginal Wall and Pelvic Floor Muscles of Rats with Simulated Birth Injury.

Vaginal delivery and resulting pelvic floor muscle (PFM) dysfunction are significant risk factors for pelvic floor dysfunction (PFD). Despite this, the biological basis underlying PFD after childbirth remain unclear. This study was aimed at assessing the early response of the vaginal wall and PFM to simulated birth injury (SBI) in rats. Forty female Sprague-Dawley rats were divided into four groups: control (sham operation), and 1, 4, and 14days post-injury. In the SBI groups, a catheter was inserted into the vagina with 130g of weight attached to the end, and the balloon was inflated to 5ml for 2h. Evaluation of vaginal tissues and PFMs included histological, immunohistochemical, Western blot, and uniaxial biomechanical testing. In the vaginal wall, the SBI group showed significantly lower COL1A1 expression and higher MMP-2 and MMP-9 expression. At 4 and 14days post-injury, there was a significant decrease in PFM fiber area and increased collagen content. The SBI group also exhibited significant increases in the expression of Nrf2, NQO1, HO-1, and SOD-2, indicating involvement of oxidative stress in both the vaginal wall and PFMs. Protein expression of Pax7 and MyoG, as well as the number of fibers with centralized nuclei, continued to increase significantly after SBI. Additionally, the vaginal wall of the SBI group showed a decreasing trend in tensile strength and elastic modulus, with a greater ultimate strain. Extracellular matrix remodeling, oxidative stress, decreased biomechanical properties, and muscle dysmyogenesis may collectively contribute to increased susceptibility to PFD development.

Age-related Changes In Markers Of Oxidative Injury In Fast And Slow Muscles Of Male And Female Rats

Age-related Changes In Markers Of Oxidative Injury In Fast And Slow Muscles Of Male And Female Rats

Impacts of endurance training and crocin supplementation on the apoptotic pathways in rat skeletal muscle following doxorubicin administration

Background and aims: Doxorubicin (DOX), in addition to its anti-cancer properties, causes toxicity and increases the apoptosis of healthy tissues. The objective of the current research was to explore the concurrent influence of an eight-week aerobic training regimen combined with crocin supplementation on the apoptosis induced by DOX within the soleus muscle tissue of male rodents. Methods: In this study, a cohort of 40 male Wistar rats, each weighing between 200 and 220 g and approximately 8 weeks old, were systematically distributed into five distinct experimental clusters, including a healthy control (normal saline) and a patient control (intraperitoneal injection of 2 mg/kg of DOX ). The other clusters were DOX-exercise (intraperitoneal injection of 2 mg/kg of DOX with eight weeks of treadmill/5 days a week), DOX-crocin (intraperitoneal injection of 2 mg/kg) 2 kg of DOX along with 10 mg/kg of crocin extract/8 weeks), and DOX-exercise-crocin. Results: The administration of DOX was associated with a notable elevation in Bax and a reduction in Bcl-2 expression (P=0.001 and P=0.001). In contrast, engaging in eight weeks of aerobic exercise, ingesting crocin, or a synergistic approach combining both interventions resulted in a marked upregulation of Bcl-2 expression (P=0.001). This combined treatment also led to a significant diminution in the Bax mRNA (P=0.006) and a decrease in the Bax/Bcl-2 ratio (P=0.001) within the soleus muscle tissue of male rodents subjected to DOX exposure. Conclusion: Aerobic exercise with crocin supplementation could inhibit apoptosis caused by DOX in the soleus muscle of male rats.

Coumarins with Different Substituents from Leonurus japonicus Have Opposite Effects on Uterine Smooth Muscle.

Leonurus japonicus Houtt is an exceptional medicinal herb used to treat obstetrical and gynecological diseases in traditional Chinese medicine, and it has significant effects on the treatment of dysmenorrhea and postpartum hemorrhage. This study investigated the effects of coumarins with diverse substituent groups from L. japonicus on isolated uterine smooth muscle and the preliminary mechanism of the most effective compound. Eight coumarins isolated from L. japonicus were assessed for their effects on the isolated uterine smooth muscle of nonpregnant rats in vitro. Coumarins 1 and 2 significantly promoted the contraction of rat uterine smooth muscle strips, whereas coumarins 3-5 showed remarkable relaxing effects against oxytocin (OT)-induced rat uterine smooth muscle contraction. Further mechanism investigations revealed that bergapten (coumarin 1) significantly increased the level of Ca2+ in uterine tissues by promoting extracellular Ca2+ influx and intracellular Ca2+ release, which were related to the activation of L-type Ca2+ channels and α-receptors. By contrast, osthole (coumarin 5), an α receptor antagonist, inhibited OT-induced uterine smooth muscle contraction by decreasing the level of Ca2+ in uterine tissues via inhibition of extracellular Ca2+ influx and intracellular Ca2+ release. This study demonstrates that the coumarins from L. japonicus are effective substances for regulating uterine smooth muscle contraction, but different coumarins with diverse substituent groups have different, even opposite effects. It can be inferred that coumarins are closely related to the efficacy of L. japonicus in the treatment of dysmenorrhea and postpartum hemorrhage.

Effects of chronic intermittent hypoxia and reoxygenation on insulin resistance and skeletal muscle miR-27a-3p/PPARγ/IRS1/PI3K/AKT expressions in rats

To investigate the effects of chronic intermittent hypoxia (CIH) and reoxygenation on insulin resistance (IR) and expressions of miR-27a-3p/PPARγ/IRS1/PI3K/AKT in rat skeletal muscle. GEO database was used for screening the differentially expressed miRNAs in CIH, and their target genes were subjected to GO and KEGG enrichment analysis followed by construction of the miRNA-mRNA-pathway regulatory network using Cytoscape. In the animal experiment, 48 male SD rats were randomly divided into normoxia group and CIH group (8 weeks of CIH followed by 4 weeks of normoxic recovery). Blood and skeletal muscle samples were collected at baseline, 8 weeks, and 12 weeks to evaluate the changes in fasting blood glucose (FBG) and fasting insulin (FINS) levels and muscular pathology. RT-qPCR and Western blotting were used to detect the changes in the expressions of miR-27a-3p, PPARγ, GLUT4, IRS1, p-IRS1, PI3K, p-AKT and AKT in the muscular tissues. No muscular miRNA datasets for CIH were available in GEO database, from which only a kidney-related dataset (GSE202480) was obtained, based on which a total of 165 differentially expressed miRNAs were identified. GO/KEGG analysis suggested that these miRNAs were involved in muscular regulation and insulin signaling. The miRNA-mRNA-pathway network highlighted miR-27a-3p as a crucial regulator in the PPAR and PI3K/AKT pathway. In the animal experiment, the rats subjected to CIH for 8 weeks showed significantly increased FBG, FINS, HOMA-IR, and PPARγ levels, loose muscle fiber arrangement, decreased cross-sectional area of the muscle fibers, and lowered expressions of miR-27a-3p, p-IRS1/IRS1, PI3K, and p-AKT/AKT in the skeletal muscles. CIH increases IR, causes skeletal muscle pathology, downregulates miR-27a-3p expression, upregulates PPARγ expression, and inhibits IRS1/PI3K/AKT insulin signaling in the skeletal muscles of rats, and these changes can be reversed by reoxygenation. MiR-27a-3p may participate in CIH-induced IR by modulating the PPAR γ/IRS1/PI3K/AKT signaling pathway.

A Novel 5-Chloro-N-Phenyl-1 H-Indole-2-carboxamide Derivative as a Glycogen Phosphorylase Inhibitor: Evaluating the Long-Term Drug Effects on Muscle Function for the First Time.

Compound 1 was previously identified by our team as a glycogen phosphorylase (GP) inhibitor with glucose-lowering activity and demonstrated to have protective effects against myocardial and cerebral ischemia. However, its impact on muscle function has not been clarified. This study is the first to evaluate the long-term effects of GP inhibitors on muscle function and metabolism. After a 28-day administration of Compound 1, we performed assays to assess muscle function and biochemical parameters in rats. We observed reductions in peak holding force, duration, tetanic contraction force, single-contraction force, and electromyographic signals under 20 s and 10 min contraction stimuli. The metabolic analysis showed no significant effects on muscle glycogen, ATP, lactic acid, and uric acid levels at low doses. In contrast, medium to high doses resulted in increased glycogen, decreased ATP, and reduced lactic acid (only at high doses), without affecting uric acid. These findings suggest that Compound 1 may adversely affect muscle function in rats, potentially due to the glycogen inhibition effects of GP inhibitors. This study provides crucial safety data and insights into the long-term effects of GP inhibitors on rat muscles, which will guide future developments and applications.

Resistance training suppresses accumulation of senescent fibro-adipogenic progenitors and senescence-associated secretory phenotype in aging rat skeletal muscle

AbstractAccumulation of senescent cells in tissues contributes to multiple aging-related pathologies. Senescent fibro-adipogenic progenitors (FAPs) contribute to aging-related muscle atrophy. Resistance training can help to maintain skeletal muscle mass, improve mobility, and reduce certain health risks commonly associated with aging. We investigated, using rat model, the impact of resistance training on FAPs in aging skeletal muscle, which remains unclear. Twenty-two-month-old female rats were divided into sedentary and training groups. The training group rodents were trained to climb a ladder while bearing a load for 20 training sessions over 2 months, after which, the flexor hallucis longus muscles were collected and analyzed. Senescent cells were identified using a senescence-associated β-galactosidase stain and p21 immunohistochemistry (IHC), and FAPs were identified using platelet-derived growth factor receptor alpha IHC. The results indicate that resistance training in rats prevented aging-associated skeletal muscle atrophy and suppressed M2 polarization of macrophages. The number of senescent cells was significantly reduced in the 24-month-old training group, with most of them being FAPs. Conversely, the number of senescent FAPs increased significantly in the 24-month-old sedentary group compared with that in the 18-month-old sedentary group. The number of senescent FAPs in the 24-month-old training group decreased significantly. Resistance training also suppressed the senescence-associated secretory phenotype (SASP). The killer T cell-specific marker, CD8α, was elevated in the skeletal muscles of the aging rats following resistance training, indicating upregulation of recognition and elimination of senescent cells. Overall, resistance training suppressed the accumulation of senescent FAPs and acquisition of SASP in aging skeletal muscles.

Remobilization with whole-body vibration improves functionality, histomorphometric parameters, and AQP1 expression in the soleus muscle of Wistar rats.

Whole-body vibration (WBV) is used to enhance physical performance in sports and rehabilitation. The present study analyzed the effects of remobilization with WBV on the soleus muscle of Wistar rats. Twenty-eight animals were separated into four experimental groups (n = 7): CON (control); IM (immobilized); FR (immobilization and free remobilization); and WBV (immobilization and remobilization with WBV). The immobilization of the pelvic limb was carried out according to the standard protocol using a plaster cast for 15 days. For remobilization with WBV, a Frequency of 60 Hz was applied for 10 min, five days a week, for two weeks. After the remobilization period, the animals were euthanized, and the right soleus muscle was dissected followed by processing for histomorphometric analysis and immunolocalization of Aquaporin 1 (AQP1). We observed a reduced larger diameter in IM compared to CON, with restored values in WBV. For the estimation of connective tissue, a significant increase was observed in the immobilized groups, while a reduction was noted in the remobilized groups. AQP1 expression decreased significantly in IM and increased in WBV. Immobilization caused morphofunctional damage to the soleus muscle, and remobilization with WBV is efficient and offers advantages over free remobilization.

Bioactive lipids are altered in the heart, kidney, and serum of male and female F344 rats sub-chronically exposed to dietary 2-MCPD

Chloropropanols have been identified as processing-induced food contaminants that occur as by-products of the manufacturing of refined food oils and hydrolyzed vegetable protein. There has been a paucity of research on the 2-monochloropropane-1,3-diol (2-MCPD) isomer, thus forming a data gap for regulatory risk assessment. Previous studies suggest 2-MCPD causes adverse cardiotoxic, nephrotoxic, and myotoxic effects, but were inconclusive for hazard identification; thus a dose-response OECD TG-408-compliant study was conducted by Health Canada. Our study profiled the effects of 2-MCPD on oxylipins and oxidized phosphatidylcholines, using HPLC-MS/MS, in heart, kidney, serum, and skeletal muscle of male and female F344 rats orally exposed to 2-MCPD (40 mg/kg BW/d) for 90 days. Cardiac n-3 polyunsaturated fatty acid-derived oxylipins, particularly DHA-derived oxylipins, were lower with 2-MCPD exposure, coincident with cardiac lesions. Lipoxygenase-derived oxylipins were decreased in the serum with a greater effect in the male 2-MCPD treatment group. Few oxylipin alterations were seen in the kidney and there was an absence of alterations in the tibialis anterior. Oxidized phosphatidylcholines and isoprostanes were not altered in this study, indicating that oxidative stress was not elevated by 2-MCPD. These findings add to the weight of the evidence for 2-MCPD toxicity and support the use of serum oxylipins as potential biomarkers of 2-MCPD exposure.

Effects of Bifidobacterium-Fermented Milk on Obesity: Improved Lipid Metabolism through Suppression of Lipogenesis and Enhanced Muscle Metabolism.

Obesity is a major global health concern. Studies suggest that the gut microflora may play a role in protecting against obesity. Probiotics, including lactic acid bacteria and Bifidobacterium, have garnered attention for their potential in obesity prevention. However, the effects of Bifidobacterium-fermented products on obesity have not been thoroughly elucidated. Bifidobacterium, which exists in the gut of animals, is known to enhance lipid metabolism. During fermentation, it produces acetic acid, which has been reported to improve glucose tolerance and insulin resistance, and exhibit anti-obesity and anti-diabetic effects. Functional foods have been very popular around the world, and fermented milk is a good candidate for enrichment with probiotics. In this study, we aim to evaluate the beneficial effects of milks fermented with Bifidobacterium strains on energy metabolism and obesity prevention. Three Bifidobacterium strains (Bif-15, Bif-30, and Bif-39), isolated from newborn human feces, were assessed for their acetic acid production and viability in milk. These strains were used to ferment milk. Otsuka-Long-Evans Tokushima Fatty (OLETF) rats administered Bif-15-fermented milk showed significantly lower weight gain compared to those in the water group. The phosphorylation of AMPK was increased and the expression of lipogenic genes was suppressed in the liver of rats given Bif-15-fermented milk. Additionally, gene expression related to respiratory metabolism was significantly increased in the soleus muscle of rats given Bif-15-fermented milk. These findings suggest that milk fermented with the Bifidobacterium strain Bif-15 can improve lipid metabolism and suppress obesity.

Protective Role of Ovothiol-A against Muscle and Kidney Injuries in Obese Rats

Background: Obesity is a serious chronic metabolic disease impairing health damaging many organs such as kidneys and muscles. Ovothiol-A (Ovo-A) has been found to keep the redox balance normal in sea urchins indicating its antioxidant characteristics. Aim: This study aims to investigate the protective effects of Ovo-A on kidneys and muscles in obese rats. objective: Investigation of the protective effect of Ovo-A on kidneys and muscles in obese rats. Methods: In-silco studies were performed on lactate dehydrogenase (LDH) and creatine kinase (CK) with Ovo-A to compute their binding affinities. Obesity was induced by high-fat diet (HFD) for 4 weeks. Wistar rats were used in this study as 6 rats per group as control, HFD, Ovo-A (200 and 400 mg/Kg, p.o) groups. Results: Docking results have revealed that Ovo-A has affinities to bind to LDH (-8.5 kcal/mol) and CK (-17.7 kcal/mol). Ovo-A reduced the levels of uric acid, urea, creatinine, LDH, CK, malondialdehyde (MDA), and nitric oxide (NO), while increasing the levels of glutathione (GSH), catalase (CAT), and glutathione-S-transferase (GST). Histopathological investigations have revealed that Ovo-A restored the renal and muscular structure. Conclusion: The current study showed that Ovo-A has a protective effect on kidneys and muscles in obese rats. Ovo-A enhances renal and muscular functions by inhibiting LDH and CK activities and improving the antioxidant system. Ovo-A is more effective in the high dose.

Composite suture material based on polylactide accelerates the healing of surgical wounds in in vivo experiment.

In laboratory conditions, composite sutures based on polylactide (PLA) containing chitin nanofibrils modified with polyethylene glycol (CN-PEG) and poviargol (silver nanoparticles stabilized with poly(N-vinylpyrrolidone)) were obtained, studied, and used as a prototype. Surgical sutures threads with the addition of CN-PEG have stable mechanical properties both in air and in a buffer simulating the environment of a living organism. The yield strength of oriented threads decreased by an average of 15%, whereas for non-oriented threads the decrease was 3-4 times. The strength values in simple units of unfilled PLA, PLA containing 5 wt % CN-PEG, and PLA with 1 wt % Poviargol were on average 50% higher than the national standard 31620-2012. The results of in vivo experiments on albino rats (cross-linking skin and muscle tissue in the linea alba area) showed that composite sutures are best for suturing muscle tissue, whereas unfilled PLA sutures are more suitable for suturing skin. When suturing muscle tissue, suturing with composite sutures increased the number of collagen fibers of different diameters.