What is the difference between rhodiola rosea and rhodiola crenulata

The malfunction of these transporters has been associated with dysfunctions in AFC, alveolar flooding, and edema. For example, alveolar hypoxia, a common phenomenon when abruptly relocating nonacclimatized individuals to a high altitude, is thought to be involved in impaired transalveolar fluid transport.

The excessive fluid that subsequently accumulates in alveoli exaggerates alveolar hypoxia and impairs gas exchange, and these processes are associated with the pathological progression of high altitude pulmonary edema HAPE , the most lethal form of high-altitude illnesses [ 3 , 4 ].

It should be noted that AFC was shown to be associated only with the protein abundance of Na,K-ATPase in the plasma membrane PM rather than the total amount in both cell and rodent models [ 6 — 8 ]. Furthermore, a large body of evidence also indicated that hypoxia is associated with impaired AFC, including mortality in studies using both in vivo and in vitro models as well as clinical studies. The phenomena that manifest during hypoxia are due in part to the hypoxia-associated malfunction of active sodium transport that results from the declined activity and expression of Na,K-ATPase [ 9 — 12 ].

Rhodiola species, a popular folk medicine in Asian and eastern European countries, have been used for the prevention of high-altitude illness and are regarded as traditional phytoadaptogens against environmental challenges in Tibet.

These species show beneficial properties, including antidepression, neuroprotective, cardioprotective, antifatigue, antihypoxia, and hepatoprotective activities.

In addition, Rhodiola species have also been reported to promote longevity and work productivity [ 15 ]. In our previous study [ 18 ], we demonstrated that Rhodiola crenulata extract RCE displayed excellent antioxidant activity and attenuated several indicators of pulmonary edema induced by hypobaric hypoxia in a rodent model. However, the effect and mechanism of Rhodiola crenulata on sodium transport in alveolar cells still needs to be elucidated.

The present study attempted to examine whether RCE, salidroside, and tyrosol are efficacious in preventing the hypoxia-mediated Na,K-ATPase endocytosis and to clarify the underlying mechanisms using both A cells and rodent models. The plant was authenticated by Dr. The dried roots of Rhodiola crenulata 2. The evaporation of the solvent under reduced pressure provided The -BuOH fraction Fraction 5 The structure of compound 1 was identified as salidroside by comparing it to the spectral data in the literature [ 19 ].

All of the experiments were carried out using cells with 3—8 passages. To allow cell differentiation for the experiments, the A cells were cultured for another 7 days after reaching confluence. A cell viability assay was performed using a cell counting kit-8 CCK-8, Dojindo, Japan , as described previously [ 20 ]. Briefly, cells were seeded in each well of the well plates and allowed to attach overnight. The PM fraction of A cells and rat lung tissues was isolated as previously described [ 22 ].

The supernatant was collected as a PM fraction. Thereafter the supernatant was collected as the PPM fraction. The same steps were followed for the normoxic control group saline. The expression of specific proteins in A cells and rat lung tissues was quantified as described previously [ 18 ].

Pretreatment with different concentrations of RCE 1. Consistently, both salidroside and tyrosol 0. As shown in Figure 2 b , the results for salidroside are , , , and -fold compared to the control NS not significant , , , and , resp.

Similarly, the results for tyrosol are , , , and -fold compared to the control NS, , , and , resp. Figure 2 c. As a positive control, NAC a thiol-reducing agent also showed the ability to alleviate the hypoxia-induced production of intracellular ROS -fold compared to the control,.

Furthermore, RCE, salidroside, and tyrosol showed no significant cytotoxicity in the dose range studied under our experimental conditions Figures 2 d , 2 e , and 2 f.

Salidroside 1. Similarly, tyrosol, which is the aglycone of salidroside, exerted potent protective effects comparable to salidroside and 0. Moreover, salidroside and tyrosol 1. On the other hand, there was no significant inductive effect on major cellular antioxidant enzymes, including SOD2 and GPx2, under hypoxic conditions, despite the fact that these enzymes were reported to provide beneficial effects for Na,K-ATPase against hypoxic insults [ 8 ].

To verify the effect of RCE in vivo , a hypobaric hypoxia rat model was employed. Salidroside and tyrosol are regarded as the major bioactive compounds and are used as the standard markers for the quantitative analysis of the quality of different Rhodiola species or preparations [ 24 ]. Until now, most studies have focused on the role of salidroside, rather than tyrosol, in the efficacy of Rhodiola species.

Thus, intensive studies about tyrosol are still lacking. In this study, we found that tyrosol, an antioxidant phenolic compound, showed antioxidant properties comparable to those of salidroside in the regulation of Na,K-ATPase via similar protective mechanisms. These results suggest that tyrosol may play a significant role in the protective effects of Rhodiola crenulata against oxidative-stress-associated disorders.

It should be noted that tyrosol also exists in wine and olive oils, two representative components of the Mediterranean diet, which have been reported to have antioxidant, anticancer, and cardiovascular benefits [ 25 , 26 ].

Thus, it is interesting to investigate whether salidroside and tyrosol have any beneficial effect for the prevention of cancer or cardiovascular disease. Using a hypobaric hypoxia rodent model, we further found that hypoxia-induced molecular responses similar to those shown in A cells and RCE exerted similar protective effects via similar mechanisms. A, which displays many characteristics of alveolar epithelial cells, is a generally accepted model of ion transport which displays great similarity to the primary rat alveolar type II ATII cells in response to hypoxia [ 27 , 28 ].

The trafficking of Na,K-ATPase under hypoxia is endocytosis from the plasma membrane to intracellular compartments first and then degradation [ 1 ]. Our results showed more rapid Na,K-ATPase degradation under hypoxia in rat lungs than in A cells Figures 5 a and 5 d , which is consistent with previous studies [ 8 , 29 ]. Thus, the results of A cells should be generally transferable to the in vivo situation. Previous evidence indicated that diminishing mitochondrial ROS via antioxidants or mitochondrial inhibitors prevented hypoxia-induced decreases in both the expression and activity of Na,K-ATPase [ 13 ].

Furthermore, we also ruled out the possibility that the reduction of intracellular ROS burden was due to cytotoxicity imparted by RCE, salidroside, and tyrosol. The anti-ROS effect of these Rhodiola products is consistent with previous studies that found that salidroside is able to decrease the oxidative stress induced by CoCl 2 , which is a hypoxia-mimicking agent, and showed protective effects against H 2 O 2 insults in different cell lines [ 31 , 32 ].

Combined with the previous findings, our results demonstrate that Rhodiola products exhibit potency in alleviating oxidative stress in different hypoxic models. Furthermore, NAC was also reported to attenuate oxidative stress and preserved Na,K-ATPase activity in an oleic-acid-induced lung injury rodent model due to its antioxidant properties [ 33 ]. Thus, our findings suggest that the protective effect of these Rhodiola products is associated with their antioxidant activity.

These results also imply that supplementation with antioxidants might help people working at high altitudes maintain AFC. AMPK is a critical metabolic sensor for energy homeostasis that regulates a large number of downstream targets. Rhodiola rosea and salidroside were shown to activate the AMPK pathway to regulate the cellular energy status in different cell lines [ 34 , 35 ].

This implied that Rhodiola products may trigger energy production by activating AMPK when organisms are in low-energy stress. The contrary effects of Rhodiola products for AMPK activation in different experimental conditions might be due to its adaptogen property, which normalizes body functions, allows the organism to adapt to environmental stresses, and prevents stressful insults from such factors [ 15 , 37 , 38 ].

Thus, Rhodiola species,which are phytoadaptogens, might act as bifunctional modulators for certain signal targets, such as AMPK, in response to different cellular conditions. Although RCE and its bioactive components show excellent antioxidant potency, the expression level of the primary antioxidant enzymes, such as SOD2 and GPx2, was not changed in our experiment Figure 3.

These results are consistent with the previous study, which indicated that Rhodiola rosea can directly ameliorate the H 2 O 2 -induced oxidative stress but not through the activation of SOD and catalase [ 39 ]. Thus, our results imply that the antioxidant activity of Rhodiola species does not primarily result from the induction of antioxidant enzymes. These findings also agree with the great radical scavenging activity of RCE, salidroside, and tyrosol, as indicated by the elimination of the 2,2-diphenylpicrylhydrazyl DPPH radical, which is a stable radical that is widely used to test the efficacy of compounds as free-radical scavengers [ 19 ].

Thus, we suggest that RCE and its bioactive components attenuate the hypoxia-mediated oxidative stress via their function as ROS scavengers instead of through the induction of antioxidant enzymes. Alveolar hypoxia is not only a pathophysiological process in HAPE but also in other inflammatory-associated respiratory disorders, such as acute lung injury and acute respiratory distress syndrome, and the severity of these disorders is related to the dysfunction of Na,K-ATPase [ 9 — 11 ].

Combined with anti-inflammatory activity [ 37 ], whether it has any beneficial effects on other hypoxia-associated respiratory disorders requires further elucidation, as there are many other ion channels that are known to be involved in transalveolar fluid transport, including ENaC [ 1 , 4 ]. It should be noted that the present study was carried out with some limitations, such as the fact that the measurement of ROS production as hypoxia-induced ROS production diminished after reoxygenation for 30 minutes [ 13 ].

Thus, the measurement needs to be processed as soon as possible in order to avoid disturbance due to reoxygenation. Zholus, V. Shervarly, et al. Spasov, A. Wikman, V. Mandrikov, et al. Tonkonogi, B. Walsh, T. Tiivel, et al. Yoshikawa, H. Shimada, H. Shimoda, et al. Tokyo , 44 , No. Wang, X. You, and F. Download references. Abidov, F. Crendal, S. Grachev, R. You can also search for this author in PubMed Google Scholar.

Reprints and Permissions. Abidov, M. Bulletin of Experimental Biology and Medicine , — Download citation. Issue Date : December Anyone you share the following link with will be able to read this content:. The Effects of Salidroside. Research identifies that salidroside may have a variety of positive effects throughout your body. Some studies show that salidroside may have adaptogenic properties. Adaptogens refer to any compound that may help your body adapt to the physical drawbacks associated with stress as well as maintaining homeostasis.

Salidroside may also support nerve health. Studies suggest that salidroside may promote nerve repair processes, regulate the release of neurotransmitters, and protect cells. One study found that salidroside may protect nerve cells from toxins and other harmful substances while promoting cognitive function. Salidroside has also been found to potentially support skeletal health as well. A study tested the effects of an isolated salidroside extract on bone. The study found that salidroside may protect against oxidative stress.

This suggests that salidroside may support bone development. Salidroside and Rosavin in Rhodiola Rosea Extracts. Many of the studies surrounding Rhodiola rosea focus on the nootropic as a whole, and the way its different phytochemicals and compounds, including rosavin and salidroside , work together. Studies show that one of the main mechanisms of action for Rhodiola rosea extract may involve its inhibition of monoamine oxidase.

Monoamine oxidase comprises a family of enzymes bound to the outer membrane of mitochondria. The various subtypes of monoamine oxidase are all involved in the oxidative breakdown of various components and neurotransmitters in your system, including dopamine, norepinephrine, and serotonin. By blocking monamine oxidase enzymes, Rhodiola rosea may potentially lead to a significant increase in certain neurotransmitters, particularly serotonin and dopamine.

By potentially increasing both dopamine and serotonin, Rhodiola rosea may support healthy stress levels and promote feelings of well-being. The increased serotonin and dopamine may also support your attention, concentration, and overall cognitive function.

Rhodiol rosea may also promote focus and mental energy. Along with its effects on certain neurotransmitters, Rhodiola rosea has been studied for its potential to regulate cortisol.

Cortisol is released during periods of physical or emotional stress. Cortisol may interfere with a healthy immune system and the normal metabolism of fats, carbohydrates, and proteins, Rhodiola rosea may support healthy cortisol and stress levels.

These adaptogenic benefits of Rhodiola rosea may also support a healthy night's sleep, which offers its own wide range of potential benefits such as promoting cognitive function. While many studies suggest that salidroside is the more powerful Rhodiola rosea supplement, both salidroside and rosavins play a key role in the potential effects of Rhodiola rosea extract.

A New Species on the Market: Rhodiola crenulata. There appear to be about species of rhodiola. The main rhodiola species of interest is rhodiola rosea as it contains both high concentrations of salidroside and rosavins.